1. 
   

   How prevalent is sleep apnea?

   
   
2. 
   

   What are the key distinguishing features between obstructive and central sleep apnea?

   
   
3. 
   

   What are the consequences of untreated sleep apnea?

   
   
4. 
   

   What are the indications for inpatient therapy for sleep apnea?

   
   
5. 
   

   How should patients with suspected sleep apnea be managed at hospital discharge?

   
   
6. 
   

   What is obesity hypoventilation syndrome and how is it best treated?

Sleep apnea is defined by repeated transient cessations of respiration during sleep. The more common type of this disorder, obstructive sleep apnea (OSA), has a prevalence approaching 5%. The burden of disease in the hospitalized patient is even greater than the general population because inpatients carry many predisposing risk factors for OSA: obesity, congestive heart failure, coronary artery disease, hypertension, stroke, and diabetes. Epidemiologic data suggest that the majority of patients with sleep apnea are undiagnosed. In 2004, national hospital discharge codes revealed fewer than 300,000 cases of sleep apnea amongst almost 35 million inpatient stays, yielding a prevalence of identified disease of less than 1%.

Although sleep apnea by itself is rarely a primary indication for hospitalization, recent evidence suggests that inpatient management of this disease needs to improve. Less than 6% of those identified as having sleep apnea in the 2004 National Hospital Discharge Survey received therapy with continuous positive airway pressure (CPAP) while in the hospital. Hospital Medicine physicians can ensure that OSA patients are identified and receive treatment. The key to identifying the possible presence of sleep apnea depends largely on an appreciation of risk factors and clinical features. Goring and Collop showed in 2008 that almost 80% of patients with suspected sleep apnea referred for a sleep study after an inpatient hospitalization were confirmed to have OSA. Therefore, inpatient identification and referral for evaluation can improve diagnosis rates and reduce the percentage of affected patients left untreated. This chapter will review the fundamentals of sleep apnea, address the management of patients with stable sleep apnea in the inpatient setting, delineate the necessity of preoperative screening in at-risk patients, and identify which patients should undergo further testing.

Sleep-disordered breathing includes two related diseases: obstructive sleep apnea and central sleep apnea—although as many as 90% of all cases are OSA. The distinction between OSA and central sleep apnea is an important one as the treatment options and responses to therapy are quite different. Obesity hypoventilation, also known as Pickwickian syndrome, is a condition in which patients afflicted with sleep apnea develop diurnal hypercapnia and hypoxemia.

Obstructive Sleep Apnea

The upper airway is a compliant structure that is also susceptible to collapse. Complex neurologic and musculoskeletal interactions cause a reduction in the cross-sectional area of the upper airway during sleep, which can result in a reduction or cessation of airflow in susceptible individuals. The imbalance between the forces that promote airway patency (the pharyngeal dilator muscles) and the negative inspiratory forces generated by the diaphragm (which promotes airway collapse) causes obstruction. The majority of patients with OSA demonstrate obstruction in the retropalatal or retrolingual areas as these locations carry the greatest risk of collapse when a negative pressure forms inside the airway during inspiration.

Even during wakefulness, the cross-sectional area of the upper airway is smaller in patients with OSA compared with disease-free controls, often the result of anatomic contributors, such as enlarged tonsils, large tongue, a high-arched palate, and abnormal positioning of the maxilla and mandible. At sleep onset, a decrease in neural output to the pharyngeal dilator muscles increases the risk of collapse. In addition, supine positioning during sleep promotes collapse by bringing the weight of external tissue to bear upon the anteroposterior diameter of the pharynx, which is usually its shortest axis (and thus the one along which collapse is most likely). Snoring, caused by a vibration of the upper airway, can be the earliest sign of obstruction, although it is a very common clinical finding (occurring in up to 40% of men and 20% of women) and has a low positive predictive value (approximately 50%) for the presence of frank sleep apnea in an otherwise unselected population.

As obstruction worsens, periods of time during which airflow is inadequate (hypopnea) or absent (apnea) occur. During these episodes there are transient increases in arterial carbon dioxide tension and decreases in arterial oxygen tension. Episodes of obstruction typically terminate in an arousal from sleep, precipitated by the changes in oxygen and carbon dioxide as well as marked pressure swings within the thoracic cavity, as the affected individual unconsciously attempts to pull in air past the obstruction, an effort that fails due to the negative pressure serving to further pull the airway walls inward, worsening collapse. The lack of restful sleep from repetitive arousals throughout the night is responsible for the symptom of excessive daytime sleepiness in affected patients. Notably, only about half of patients with sleep apnea report overt sleepiness; others may report symptoms of fatigue, lack of energy, or other related symptoms without frank sleepiness.

Central Sleep Apnea

Several mechanisms contribute to the pathophysiology of central sleep apnea. Central events are marked by a transient absence of respiratory effort. Affected patients fall into two main groups, those with daytime hypercapnia and those without. All human beings have a slight decline in respiratory drive during sleep, with a typical increase in pCO2 of about 5 mm of mercury; this change is normally achieved through a transient period of hypoventilation at sleep onset. Amongst patients with daytime hypoventilation (including those with chronic obstructive pulmonary disease and a number of neuromuscular disorders), an already impaired ventilatory drive is further suppressed, causing apnea.

Normocapneic patients with central apnea have a longer period of hypoventilation than is normally present at sleep onset. Circulatory delay, common in heart failure and often associated with central apnea, increases the amount of time it takes for carbon dioxide sensors in the medulla to appreciate the effect of a change in minute ventilation. Overshoot hypercapnia and subsequent tachypnea in an effort to reduce carbon dioxide levels leads to arousal.

The other major mechanism of central sleep apnea requires that the central apnea patient demonstrate a change in minute ventilation out of proportion to that which would be needed to correct a change in the partial pressure of carbon dioxide. Affected patients will have a prolonged period of hypoventilation at sleep onset, occasionally leading to arousal from overshoot hypercarbia and associated hypoxia. In both of these cases, Cheyne-Stokes respiration (also known as periodic breathing) can occur, characterized by a fluctuation in breathing apnea and tachypnea with a crescendo-decrescendo morphology.

When evaluating patients for possible OSA, the symptom-based differential diagnosis can be broad (Table 242-1). While history may be highly suggestive of OSA, several other disorders can mimic its symptoms. Central sleep apnea presents with witnessed breathing pauses at night and daytime fatigue, although the mechanism of disease and appropriate treatment is quite different. Other causes of frequent nocturnal arousals and daytime somnolence include periodic limb movement disorder, prostatism and environmental sleep disorder, in which a stimulus external to the patient causes recurrent sleep disruption. Patients with nocturnal pain and inadequately controlled mood disorders may also demonstrate frequent nocturnal arousals. Excessive daytime sleepiness can be a symptom of insufficient sleep (the most common cause of daytime somnolence), depression, narcolepsy and idiopathic hypersomnia, as well as a number of endocrinologic, cardiac, pulmonary, renal, and hematologic disorders.

Snoring does not necessarily equate to sleep apnea. Primary snoring, while a socially difficult condition, has not clearly been associated with any long-term health repercussions. Patients who awaken with paroxysmal dyspnea at night may also suffer from congestive heart failure, chronic obstructive pulmonary disease, nocturnal gastroesophageal reflux or nocturnal panic attacks. A small percentage of patients with severe sleep apnea will demonstrate diurnal hypercapnia, although the diagnoses of underlying pulmonary disease (either restrictive or obstructive) and neuromuscular disease affecting the muscles of respiration should also be entertained.

Patients with OSA present to the hospital with other medical problems and the clinician must identify at-risk patients so that they might undergo appropriate evaluation. Older age, obesity, and male sex are the most significant risk factors for OSA. Because the prevalence of these characteristics in the general population is too high for them to be useful as a screening tool, history and physical examination are critical in determining which patients are appropriate referrals for sleep testing (Table 242-2).

A screening history for OSA includes an assessment of both nocturnal and diurnal symptoms, and the accuracy of the history improves if the patient’s bed partner is available for questioning as that person can offer greater insight into events that occur when the patient is unconscious. Snoring is the most common symptom of obstructive sleep apnea, present in more than 90% of patients with the disease, suggesting that the absence of snoring (by history from bed partner or other witness) would have a good negative predictive value for OSA. The presence of witnessed apneas, seen in 75% of patients with OSA, has a positive predictive value of greater than 80% for the presence of sleep apnea, although data do not suggest their presence can indicate the severity of the disease. The absence of witnessed apneas, does not reliably exclude the diagnosis of OSA, however. Another suggestive clue in the history includes waking up with a sensation of choking or gasping for air. This symptom usually represents an arousal from an apneic episode, with the sensation normally subsiding within seconds of waking. Rarely, patients may complain of insomnia (which probably represents disturbed sleep secondary to arousal), although the majority of patients report no difficulty initiating sleep. Nocturia

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