Course Authors

Ahmed Syed Ali, M.D., and John E. Morley, M.D.

Dr. Ali is a visiting scientist in the Division of Geriatric Medicine at Saint Louis University Health Science Center. Dr. Ali reports no commercial conflict of interest. During the last three years, Dr. Morley has received grant/research support from Vivus, Merck & Co., Upjohn, B. Braun McGaw, Bayer Corp and Nestec, Ltd. He has also served on the Speakers' Bureau for LXN, Organon, Ross, Pharmacia & Upjohn, Glaxo Wellcome, Hoechst Marion Roussel, Searle, Merck & Co., Roche, Bristol-Myers Squibb, Novartis, Pratt, B. Braun McGaw, Pfizer and Parke-Davis.

This activity is made possible by an unrestricted educational grant from the Novartis Foundation for Gerontology.

Estimated course time: 1 hour(s).

Albert Einstein College of Medicine – Montefiore Medical Center designates this enduring material activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

In support of improving patient care, this activity has been planned and implemented by Albert Einstein College of Medicine-Montefiore Medical Center and InterMDnet. Albert Einstein College of Medicine – Montefiore Medical Center is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.

 

Learning Objectives

Upon completion of this Cyberounds^®, you should be able to:

• Recognize the importance of sleep apnea in older persons

• Identify the risk factors for sleep apnea

• Diagnose and treat sleep apnea.

 

Peto: Falstaff is fast asleep behind the arris and snorting like a horse.

Prince: Hark! How hard he fetches breath.

Shakespeare's Henry IV, Part I, Act II, Scene 4

The term "sleep apnea" means temporary absence or cessation of breathing (airflow) during sleep, occurring at least 30 times during the night. Airflow must be absent for some arbitrary period of time, longer than the usual inter-breathing interval. This is defined as ten seconds for adults. Sleep apnea has been reported to be extremely common in older persons, with either sleep apnea or hypopnea occurring in at least 50% of persons over 60 years.(1) In comparison, sleep apnea occurs in 6% of middle aged females and 9% of males.

Classifications

Central Sleep Apnea (CSA)

In CSA, there is periodic cessation of respiratory muscle activity. Pure CSA is uncommon; it occurs in patients with primary hypoventilation or in patients with a brain stem lesion. Cheyne-Strokes respiration, an accentuated form of periodic breathing with apnea, is a form of central sleep apnea found in patients with congestive heart failure, stroke or uremia. Recently, it was suggested that enhanced sensitivity to carbon dioxide might play a pivotol role in the development of CSA.(2)

Obstructive Sleep Apnea (OSA)

This is the most common form of sleep apnea. In OSA, there is ventilatory effort but no airflow because the upper airway is transiently closed (at the level of pharynx).

Mixed Sleep Apnea (MSA)

There is, initially, no ventilatory effort, which is then followed by an obstructive apnea pattern that is evident when effort resumes.

Hypopnea

Hypopnea is a temporary decrease in inspiratory airflow. In clinical practice, it can be defined as a decrement in airflow, with drop in oxyhemoglobin saturation of at least 4%. Hypopnea, like apneas, can be central or obstructive. In sleep studies reports, this distinction is rarely made.

Apnea Index

The apnea index is obtained by dividing the total number of apneic periods, during a recording period, by the total sleep time, i.e., the average number of apneic episodes per hour of sleep.

Obstructive Sleep Apnea

In OSA, the most common form of sleep apnea, episodes of apnea occur during sleep as a result of upper airway obstruction. The site of obstruction may be anywhere from the nose to glottis. Most frequently, the primary obstruction occurs in the nasopharynx, at the level of the soft palate.

Historical Background

Oslar and Burwell(3) named the combination of obesity, hypersomnolence and the sign of chronic alveolar hypoventilation as "Pickwickian Syndrome," after the fictional character from Charles Dickens of the same name. Both central and obstructive apnea had been noted by bedside observation during sleep as early as 1877.(3)

An illustration was published in 1964 showing obstructive apnea in an obese, hypersomnolent, myxedematous female. In 1965, Gastaut and co-workers(4) simultaneously recorded sleep, electrophysiologically, and breathing in a patient with the "Pickwickian Syndrome" and described all three types of apneas. In 1969, treatment of OSA by tracheostomy was described. Subsequent research discovered the details of the pathophysiology of sleep apnea and has expanded the clinical picture to include sleep disturbed by more subtle degrees of upper airway narrowing.

Epidemiology

OSA is a common disorder.(5) In the USA, more than three million men and one and a half million women meet at least one definition of OSA (Apnea/hypopnea Index of five or more plus a component of daytime sleepiness).

Pathophysiology

The pharynx is smaller in size than normal and/or demonstrates abnormal collapsibility in patients with OSA. The pharynx must be collapsible because, as an organ for speech and deglutition, it must be able to change shape and close. However, as a conduit of airflow, it must resist collapse. These functions are controlled by a group of muscles that can alter the shape of the pharynx when we swallow or talk but will hold it open when we inhale. Sleep interferes with all these functions.

The following physiologic changes are seen with sleep:(6)

1. Reduced tonic input to upper airway muscles.
2. Diminished reflexes that protect the pharynx from collapse.
3. Reduced load compensation.
4. An increased chemoreceptor "set point" during non-REM sleep which reveals a sensitive hypocapnia-induced apneic threshold.

Since all these factors are interactive, sleep is associated with pharyngeal narrowing and a substantial increase in inspiratory resistance, even in normal individuals. An abnormal pharynx can be kept open during wakefulness by an appropriate compensatory increase in dilator muscle activity(6) but, during sleep, this compensation fails and the airway collapses. Partial collapse results in snoring, hypopneas and, in some cases, prolonged hypoventilation. Complete closure results in an apnea.

Termination of Apnea

In order to terminate the sleep apnea, spells of arousal are required for the return of sufficient pharyngeal dilator muscle activity and adequate airflow. How these arousals are initiated is still unknown. One possible explanation may be related and proportional to the total increase in the "drive" to breathe. Another explanation is that they may occur in response to dyspnea, the respiratory equivalent of pain. Repetitive arousals result in sleep fragmentation and are the primary cause of hypersomnolence during the day.

Risk Factors

Risk factors include:

1. Anatomically narrowed airways, e.g., micrognathia, macroglossia, obesity and tonsillar hypertrophy.
2. Ingesting alcohol or a sedative before going to bed. Moderate alcohol intake at bedtime can produce sleep apnea episodes (10-20 nightly) in healthy men.
3. Nasal obstruction of any type including the common cold.
4. Hypothyroidism and cigarette smoking.

Secondary Complications

• Cardiac arrhythmias, particularly bradyarrhythmias, such as sinus bradycardia, sinus arrest or atrio-ventricular block, can be seen with apneas. Tachyarrythmias, including paroxysmal supraventicular tachycardia, atrial fibrillation and ventricular tachycardia, are common once airflow is re-established.
• Severe hypoxemia during apneic episodes.
• Daytime consequences of nocturnal hypoxemia, including congestive heart failure, pulmonary hypertension, cor pulmonale and secondary erythrocytosis.
• Increased prevalence of systemic hypertension.
• Retrospective studies show patients with sleep apnea are at increased risk for early death but, not necessarily, during sleep. In nursing homes, females with sleep apnea are especially prone to premature death.
• Accelerated atherosclerosis and myocardial infraction are associated with sleep apnea, secondary to hypoxic induced increase in circulating catecholeamines leading to an increase in intracellular adhesion molecule 1(ICAM-1) and L-selectin.(7) These molecules appear to be important in the pathogenesis of the leading inflammatory component of atherosclerosis. They promote leukocyte adhesion to the endothelium.

Presentation

It is usually the bed partner who provides the motivation for the patient's first visit to the clinician. Typically, the patient with OSA is a male who is moderately obese and hypertensive with a chief complaint of:

• Morning dry mouth or sore throat
• Personality change, moodiness, lack of concentration
• Morning confusion
• Intellectual impairment, with a decreased short-term memory
• Impotence and decreased libido
• Morning headaches
• Gastro-esophageal reflux
• Drowsiness during the day
• Decreased vigilance while driving, resulting in motor vehicle accidents.
• Obstructive Sleep Apnea syndrome can be suspected when the (Epworth Sleepiness Score) is 12 or greater.

Physical Examination

The typical patient is a hypertensive, obese, middle-aged or older man with a large neck (collar size of >17.5) and a structurally abnormal or " crowded" upper airway. However, OSA may be more common in females than previously thought, with a prevalence in general population of 2% (compared with 4% in men).

Obstruction in the upper airway, such as severe nasal obstruction (DNS), low hanging soft palate and a large uvula, enlarged tonsils/adenoids, macroglossia, and retroganthia or microganthia, may be present. Nasopharyngeal tumors are rare but must be considered as a cause of OSA.

Other uncommon contributory disorders include hypothyroidism, acromegaly, amyloidosis, neuromuscular disease, vocal cord paralysis, poliomyelitis, Marfan's syndrome and mucopolysaccharidoses.

Initial Laboratory Workup

1. Screening for hypothyroidism, by obtaining a TSH, is especially important in elderly OSA patients.
2. Greater than two plus proteinuria in 2% of patients may be severe enough to be in the nephrotic range.
3. Arterial blood gases to detect hypoxemia.
4. An EKG to detect arrhythmias (bradyarrhythmias) or complete heart block.
5. Nuclear radiographic studies to detect cor pulmonale.
6. Hemoglobin to exclude polycythemia.

Indications for Further Evaluation for the Diagnosis of OSA

Clinical features do not reliably predict sleep apnea in patients suspected of having the disorder.(8) Several models have been developed which can help the clinician decide which patients need to be referred for more definitive testing.(9),(10)

The following four clinical variables were combined in a linear model to give a "Sleep Apnea Clinical Score":(10)

1. Presence or absence of hypertension (or hypertension treatment)
2. Neck circumference (or collar size)
3. History of habitual snoring
4. Observed reports of nocturnal choking or gasping

A score <10 has a very low post-test probability of having important sleep apnea and does not need further evaluation.

A score >15 has a high probability of having clinically important sleep apnea and require further testing.

Scores between 10 and 15 might be potential candidates for a home apnea test.

There are several tests, models and algorithms but none can substitute for clinical judgment. It is recommended that all patients with an otherwise unexplained complaint of excessive daytime sleepiness deserve further evaluation. A sleepy, stentorian snorer who has had witnessed apneas probably should be examined during sleep regardless of the size of his or her neck.

Diagnosis

Polysomnography is the test of choice for suspected OSA. This test monitors multiple physiological factors during sleep (e.g., sleep, heart rate and respiratory movement; oxygen saturation studies).

Otolaryngological examination, electroencephalography, electroocculography, electromyography, electrocardiography, oximetry and measurement of respiratory effort and airflow are performed in a complete evaluation.

Non-Surgical Treatment

Behavioral

1. Dietary modification for weight loss
2. Restriction of body position during sleep
3. Avoidance of alcohol and other substances known to make apnea worse
4. Avoidance of upper airway mucosal irritants
5. Possibly avoidance of high altitude

Pharmacological

A variety of drugs have been tried but the results have not been encouraging:

1. Nasal decongestant or steroids to increase upper airway patency.
2. Medroxyprogesterone acetate and acetazolamide to produce respiratory stimulation.
3. A tricyclic antidepressant, protriptiline 10-20 mg qhs, is helpful in a small number of patients.
4. Supplemental O₂ in those who sleep in high altitude environments may lessen the severity of nocturnal desaturation but may also lengthen the apneas. Polysomnography is necessary to assess the effect of oxygen therapy.

Mechanical Devices

Orthodontic devices (which hold the lower jaw forward) and tongue retaining appliances (which hold the tongue forward). Both of these devices are useful in those patients with mild or positional apnea.

In 1981, sleep apnea was reported to be cured by utilizing a vacuum-cleaner blower motor which blew air through silastic tubing into the nose.(11) Nasal continuous positive airway pressure (CPAP) has been a major advance in mechanical treatment and has largely replaced tracheostomy. Polysomnography is necessary to determine what level of CPAP (usually 5-15 cm H₂O) is necessary to abolish obstructive apneas. Patients must use CPAP system nightly. Unfortunately, only 75% of patients continue to use nasal CPAP for more than one year.

Surgical Treatment

Uvulopalatopharyngoplasty -- resection of pharyngeal soft tissue and amputation of approximately 15 mm of the free edge of the soft palate and uvula -- is helpful in patients with retropalatal airway occlusion (only half of operations are successful).

Tonsillectomies, with or without adenoidectomy, and nasal septoplasty are commonly used procedures to relieve upper airways obstruction.

Tracheostomy was the first and definitive treatment used for OSA but it has numerous adverse effects, including granuloma formation, difficulty with speech, and stoma and airway infection. Tracheostomy and other maxiollofacial surgery approaches are reserved for patients with life-threatening arrhythmias or severe disability who have failed to respond to conservative therapy.

New advances in surgical techniques in the treatment of OSA include:

1. Advancement genioplasty (a.k.a. anterior mandibular horizontal osteotomy), modified block osteotomy to anteriorly reposition only the genial tubercles and their muscular attachments, and bilateral sagittal split ramus osteotomies (BSSRO) for mandibular advancement. Occasionally, patients with normal maxillomandibular relations may be treated with advancement of both jaws (BSSRO and Le Fort I +/- advancement genioplasty +/- hyoid resuspension) though esthetic effects may be negative. (Courtesy of Kim E. Goldman, D.M.D.)
2. Maxillomandibular and hyoid advancement by Riley and Powell.
3. Laser midline glossectomy by Fujita and colleagues.
4. Direct electrical stimulation of hypoglossal nerve can improve airflow in patients with obstructive sleep apnea.(12)
5. TBRHE (Tongue Based Reduction with Hyoepiglottoplasty)(13) is a safe procedure for the neurovascular bundle. Associated to a pharyngotomy, it is an effective treatment for severe obstructive sleep apnea attributable to tongue base obstruction.

Summary

Sleep apnea is an extremely common, treatable condition in older persons. Failure to treat can result in severe co-morbidities. Physicians need to screen for sleep apnea on a regular basis in their older patients.