Obstructive sleep apnea/hypopnea syndrome (OSAHS) is one of the most important medical conditions identified in the last 50 years. It is a major cause of morbidity, a significant cause of mortality throughout the world, and the most common medical cause of daytime sleepiness. Central sleep apnea is a less common clinical problem. Other sleep disorders are discussed in Chap. 28.
Definition
OSAHS may be defined as the coexistence of unexplained excessive daytime sleepiness with at least five obstructed breathing events (apnea or hypopnea) per hour of sleep (Table 259-1). This event threshold may need to be refined upward in the elderly. Apneas are defined in adults as breathing pauses lasting 10 s and hypopneas as 10 s events where there is continued breathing but the ventilation is reduced by at least 50% from the previous baseline during sleep. As a syndrome, OSAHS is the association of a clinical picture with specific abnormalities on testing; asymptomatic individuals with abnormal breathing during sleep should not be labeled as having OSAHS.
Table 259-1 Clinical Indicators in the Sleepy Patient
OSAHS Narcolepsy IHS
Age of onset (years) 35–60 10–30 10–30
Cataplexy No Yes No
Night sleep
Duration Normal Normal Long
Awakenings Occasional Frequent Rare
Snoring Yes, loud Occasional Occasional
Morning drunkenness Occasional Occasional Common
Daytime naps
Frequency Usually few Many Few
Time of day Afternoon/evening Afternoon/evening Morning
Duration <1 h <1 h >1 h
Note: Features suggesting obstructive sleep apnea/hypopnea syndrome (OSAHS), narcolepsy, or idiopathic hypersomnolence (IHS).
Mechanism of Obstruction
Apneas and hypopneas are caused by the airway being sucked closed on inspiration during sleep. This occurs as the upper-airway dilating muscles—like all striated muscles—normally relax during sleep. In patients with OSAHS, the dilating muscles can no longer successfully oppose negative pressure within the airway during inspiration. The primary defect is not in the upper-airway muscles, which function normally in OSAHS patients when awake. These patients have narrow upper airways already during wakefulness, but when they are awake their airway dilating muscles have higher than normal activity, which ensures airway patency. However, when they are asleep, muscle tone falls and the airway narrows; snoring may commence before the airway occludes, and apnea results. Apneas and hypopneas terminate when the subject arouses, i.e., wakens briefly, from sleep. This arousal is sometimes too subtle to be seen on the electroencephalogram but may be detected by cardiac acceleration, blood pressure elevation, or sympathetic tone increase. The arousal results in return of upper-airway dilating muscle tone, and thus airway patency is resumed.
The factors predisposing to OSAHS by narrowing the pharynx include obesity—around 50% have a body mass index (BMI) >30 kg/m2 in western populations—and shortening of the mandible and/or maxilla. This change in jaw shape may be subtle and can be familial. Hypothyroidism and acromegaly predispose to OSAHS by narrowing the upper airway with tissue infiltration. Other predisposing factors for OSAHS include male gender and middle age (40–65 years), myotonic dystrophy, Ehlers Danlos syndrome, and perhaps also smoking.
Epidemiology
Broadly, the frequency of OSAHS is in the range of 1–4% of the middle-aged male population; it is around half as common in women. The syndrome also occurs in childhood–usually associated with tonsil or adenoid enlargement–and in the elderly, although the frequency is slightly lower in old age. Irregular breathing during sleep without daytime sleepiness is much more common, occurring in perhaps one-fourth of the middle-aged male population. However, as these individuals are asymptomatic, they do not have OSAHS and there is no evidence at present that these events are harmful.
Clinical Features
Randomized controlled treatment trials have shown that OSAHS causes daytime sleepiness; impaired vigilance, cognitive performance, and driving; depression; disturbed sleep; and hypertension. Daytime sleepiness may range from mild to irresistible, and the sleep attacks can be indistinguishable from those in narcolepsy (Chap. 28). The sleepiness may result in inability to work effectively and may damage interpersonal relationships and prevent socializing. The somnolence is dangerous when driving, with a three- to sixfold risk in accidents on the road or when operating machinery. Experiments with normal subjects repeatedly aroused from sleep indicate that the sleepiness results, at least in part, from the repetitive sleep disruption associated with the breathing abnormality. The possible contribution from the recurrent hypoxemia requires further evaluation.
Other symptoms include difficulty concentrating, unrefreshing nocturnal sleep, nocturnal choking, nocturia, and decreased libido. Partners report nightly loud snoring in all postures, which may be punctuated by the silence of apneas. Partners often give a markedly different assessment of the extent of sleepiness.
Cardiovascular and Cerebrovascular Events
OSAHS raises 24-h mean blood pressure. The increase is greater in those with recurrent nocturnal hypoxemia, is at least 4–5 mmHg, and may be as great as 10 mmHg in those with >20% arterial oxygen desaturations per hour of sleep. This rise probably results from a combination of surges in blood pressure accompanying each arousal from sleep that end each apnea or hypopnea and from the associated 24-h increases in sympathetic tone.
Epidemiologic data in normal populations indicate that this rise in blood pressure would increase the risk of myocardial infarction by around 20% and stroke by about 40%. While there are no long-term randomized controlled trials to indicate whether this is true in OSAHS patients—and such studies would not be ethically defensible—observational studies suggest an increase in the risk of myocardial infarction and stroke in untreated OSAHS. Furthermore, epidemiologic studies suggest, but do not prove, increased vascular risk in normal subjects with raised apneas and hypopneas during sleep. Patients with recent stroke have a high frequency of apneas and hypopneas during sleep. These seem largely to be a consequence, not a cause, of the stroke and to decline over the weeks after the vascular event. There is no evidence that treating the apneas and hypopneas improves stroke outcome.
There has been debate for decades whether OSAHS is an adult form of sudden infant death syndrome. Although earlier studies showed no increase in sudden nocturnal deaths in OSAHS, a recent large study reported excess nocturnal deaths in subjects previously shown to have apneas and hypopneas during sleep.
Diabetes Mellitus
The association of OSAHS with diabetes mellitus is not just due to obesity being common in both conditions. Recent data suggest that increased apneas and hypopneas during sleep are associated with insulin resistance independent of obesity. In addition, uncontrolled trials suggest that OSAHS can aggravate diabetes and that treatment of OSAHS in patients who also have diabetes decreases their insulin requirements.
Liver
Hepatic dysfunction has also been associated with irregular breathing during sleep. Non-alcohol drinking subjects with apneas and hypopneas during sleep were found to have raised liver enzymes and more steatosis and fibrosis on liver biopsy, independent of body weight.
Anesthestic Risk
Patients with OSAHS are at increased risk perioperatively as their upper airway may obstruct during the recovery period or as a consequence of sedation. Patients whose anesthesiologists have difficulty intubating are much more likely to have irregular breathing during sleep. Anesthesiologists should thus take sleep histories on patients preoperatively and take the appropriate precautions with those who might have OSAHS. This should include referring patients suspected of having OSAHS for investigation, and some elective operations may need to be postponed until the OSAHS is treated.
Differential Diagnosis
(See also Chap. 28) Causes of sleepiness which may need to be distinguished include (Table 259-1):
Insufficient sleep: this can usually be diagnosed by history.
Shift work: this is a major cause of sleepiness, especially in those over 40 years old on either rotating shift or night shift work patterns.
Psychological/psychiatric causes: depression is a major cause of sleepiness.
Drugs: both stimulant and sedative drugs can produce sleepiness.
Narcolepsy: around 50 times less common than OSAHS, narcolepsy is usually evident from childhood or teens and is associated with cataplexy.
Idiopathic hypersomnolence: this is an ill-defined condition typified by long sleep duration and sleepiness.
Phase alteration syndromes: both the phase delay and the less-common phase advancement syndromes are characterized by sleepiness at the characteristic time of day.
WHO to Refer for Diagnosis
Anyone whose troublesome sleepiness is not readily explained and rectified by considering the above differential diagnosis should be referred to a sleep specialist. The guideline I use for patients with troublesome sleepiness includes those with an Epworth Sleepiness Score >11 (Table 259-2), and those for whom sleepiness during work or driving poses problems. However, the Epworth Score is not a perfect measure for detecting troublesome sleepiness, as many whose life is troubled by frequently fighting sleepiness but who never doze will correctly score themselves as having a low Epworth Score. The patient and his/her partner often give divergent scores for the patient's sleepiness, and in such cases the higher of the two scores should be used.
Table 259-2 Epworth Sleepiness Score
How often are you likely to doze off or fall asleep in the following situations, in contrast to feeling just tired? This refers to your usual way of life in recent times. Even if you have not done some of these things recently, try to work out how they would have affected you. Use the following scale to choose the most appropriate number for each situation:
0 = would never doze
1 = slight chance of dozing
2 = moderate chance of dozing
3 = high chance of dozing
Sitting and reading . . .. . .. . .. . .. . ..
Watching TV . . .. . .. . .. . .. . ..
Sitting, inactive in a public place (e.g., a theater or a meeting) . . .. . .. . .. . .. . ..
As a passenger in a car for an hour without a break . . .. . .. . .. . .. . ..
Lying down to rest in the afternoon when circumstances permit . . .. . .. . .. . .. . ..
Sitting and talking to someone . . .. . .. . .. . .. . ..
Sitting quietly after lunch without alcohol . . .. . .. . .. . .. . ..
In a car, while stopped for a few minutes in traffic . . .. . .. . .. . .. . ..
TOTAL . . .. . .. . .. . .. . .
Source: From MW Johns: Sleep 14:540, 1991.
Diagnosis
OSAHS is a condition requiring lifelong treatment, and the diagnosis needs to be made or excluded with certainty, when possible, by a specialist. This will hinge on obtaining a good sleep history from the patient and partner, including asking both to complete sleep questionnaires, including the Epworth Sleepiness Score (Table 259-2). Physical examination must include assessment of obesity, jaw structure, the upper airway, blood pressure, and possible predisposing causes, including hypothyroidism and acromegaly (see above).
In those with appropriate clinical features, the diagnostic test must demonstrate recurrent breathing pauses during sleep. This may be a full polysomnographic examination with recording of multiple respiratory and neurophysiologic signals during sleep (Chap. 28). Increasingly, and especially outside the United States, most diagnostic tests are "limited studies"—recording respiratory and oxygenation patterns overnight without neurophysiologic recording. Such approaches in expert hands produce good patient outcomes and are cost-effective. It is sensible to use such limited sleep studies as the first-line diagnostic test and then allow positively diagnosed patients to proceed to treatment. However, a reasonable approach at present is for patients with troublesome sleepiness but negative limited studies to then have polysomnography to exclude or confirm OSAHS.
Obstructive Sleep Apnea: Treatment
Whom to Treat
There is evidence obtained from robust randomized controlled trials (RCT) that treatment improves symptoms, sleepiness, driving, cognition, mood, quality of life, and blood pressure in patients who have an Epworth score of >11, troublesome sleepiness while driving or working, and >15 apneas + hypopneas per hour of sleep. For those with similar degrees of sleepiness and 5–15 events per hour of sleep, RCTs indicate improvements in symptoms, including subjective sleepiness, with less strong evidence indicating gains in cognition and quality of life. There is no evidence of blood pressure improvements in this group, nor is there is evidence that treating nonsleepy subjects improves their symptoms, function, or blood pressure. Thus, treatment cannot be advocated for this large group.
How to Treat
All patients diagnosed with OSAHS should have the condition and its significance explained to them and to their partner. This should be accompanied by provision of written and/or web-based information and a discussion of the implications of the local regulations for driving. Rectifiable predispositions should be discussed; this often includes weight loss and sometimes reduction of alcohol consumption to reduce caloric intake and because alcohol acutely decreases upper-airway dilating muscle tone, thus predisposing to obstructed breathing. Sedative drugs, which also affect airway tone, should be carefully withdrawn.
Continuous Positive Airway Pressure (CPAP)
CPAP therapy works by blowing the airway open during sleep, usually with pressures of 5–20 cmHg. CPAP has been shown in randomized placebo-controlled trials to improve breathing during sleep, sleep quality, sleepiness, blood pressure, vigilance, cognition, and driving ability, as well as mood and quality of life in patients with OSAHS. However, this is obtrusive therapy, and care must be taken to explain the need for the treatment to the patient and his/her partner, and to support all patients on CPAP intensively, providing access to telephone support and regular follow-up. Initiation should include finding the most comfortable mask from the ranges of several manufacturers and trying the system for at least 30 min during the daytime to prepare for the overnight trial. An overnight monitored trial of CPAP is used to identify the pressure required to keep the patient's airway patent. The development of pressure-varying CPAP machines may make the in-lab CPAP night trial unnecessary, but treatment must be initiated in a supportive environment. Thereafter, patients can be treated with fixed-pressure CPAP machines set at the determined pressure or by a self-adjusting, intelligent CPAP device. The main side effect of CPAP is airway drying, which can be countered using an integral heated humidifier. CPAP use, like that of all therapies, is imperfect, but around 94% of patients with severe OSAHS are still using their therapy after 5 years on objective monitoring.
Mandibular Repositioning Splint (MRS)
Also called oral devices, MRSs work by holding the lower jaw and the tongue forward, thereby widening the pharyngeal airway. MRSs have been shown in RCTs to improve OSAHS patients' breathing during sleep, daytime somnolence, and blood pressure. As there are many devices of differing design with unknown relative efficacy, these results cannot be generalized to all MRSs. Self-reports of the use of devices long-term suggest high dropout rates.
Surgery
Four forms of surgery have a role in OSAHS, although it must always be remembered that these patients have a raised perioperative risk. Bariatric surgery can be curative in the morbidly obese. Tonsillectomy can be highly effective in children but rarely in adults. Tracheostomy is curative but rarely used because of the associated morbidity; nevertheless, it should not be overlooked in extremely advanced cases. Jaw advancement surgery—particularly maxillo-mandibular osteotomy—is effective in those with retrognathia (posterior displacement of the mandible) and should be particularly considered in young and thin patients. There is no robust evidence that pharyngeal surgery, including uvulopalatopharyngoplasty (whether by scalpel, laser, or thermal techniques) helps OSAHS.
Drugs
Unfortunately, no drugs are clinically useful in the prevention or reduction of apneas and hypopneas. A marginal improvement in sleepiness in patients who remain sleepy despite CPAP can be produced by modafinil, but the clinical value is debatable and the financial cost significant.
Choice of Treatment
CPAP and MRS are the two most widely used and best evidence-based therapies. Direct comparisons in RCTs indicate better outcomes with CPAP in terms of apneas and hypopneas, nocturnal oxygenation, symptoms, quality of life, mood, and vigilance. Adherence to CPAP is generally better than to an MRS, and there is evidence that CPAP improves driving, whereas there are no such data on MRSs, Thus, CPAP is the current treatment of choice. However, MRSs are evidence-based second-line therapy in those who fail CPAP. In younger, thinner patients, maxillo-mandibular advancement should be considered.
Health Resources
Untreated OSAHS patients are heavy users of health care and dangerous drivers; they also work beneath their potential. Treatment of OSAHS with CPAP is cost-effective in terms of reducing health care costs of associated illness and associated accidents.
Central Sleep Apnea
Central sleep apneas (CSAs) are respiratory pauses caused by lack of respiratory effort. These occur occasionally in normal subjects, particularly at sleep onset and in REM sleep, and are transiently increased following ascent to altitude. Recurrent CSA is most commonly found in the presence of cardiac failure or neurologic disease, especially stroke. Spontaneous central sleep syndrome is rare and can be classified on the basis of the arterial PCO2.
Hypercapnic CSA occurs in conjunction with diminished ventilatory drive in Ondine's curse (central alveolar hypoventilation). Patients with normocapnic spontaneous CSA have a normal or low arterial PCO2 when awake, with brisk ventilatory responses to hypercapnia. This combination results in unstable ventilatory control, with subjects breathing close to or below their apneic threshold for PCO2 during sleep; this apneic tendency is compounded by cycles of arousal-induced hyperventilation, inducing further hypocapnia.
Clinical Features
Patients may present with sleep maintenance insomnia, which is relatively unusual in OSAHS. Daytime sleepiness may occur.
Investigation
Many apneas previously labeled central because of absent thoracoabdominal movement are actually obstructive, identification of movement being particularly difficult in the very obese. CSA can only be identified with certainty if either esophageal pressure or respiratory muscle electromyography is recorded and shown to be absent during the events.
Central Sleep Apnea: Treatment
Patients with underlying cardiac failure should have their failure treated appropriately. CPAP may improve outcome but is difficult to initiate and has not been shown to improve survival. Patients with spontaneous normocapnic CSA may be successfully treated with acetazolamide. In a minority of patients, CPAP is effective, perhaps because in some patients with OSAHS, pharyngeal collapse initiates reflex inhibition of respiration, and these episodes are prevented by CPAP. Oxygen and nocturnal nasal positive/pressure ventilation may also be tried.
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