Sleep Disorders

Obstructive Sleep Apnea

Obstructive sleep apnea/hypopnea syndrome (OSAHS)

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

Definition 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

This event threshold may need to be refined upward in the elderly

Apneas are defined in adults as breathing pauses lasting 10s hypopneas are defined as 10s 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 association of a clinical picture with specific abnormalities on testing

asymptomatic individuals with abnormal breathing during sleep should not be labeled as having

OSAHS

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

Mechanism of Obstruction Apneas/hypopneas are caused by the airway being sucked closed on

inspiration during sleep occurs as 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 primary defect is not in upper-airway muscles, which function normally

in OSAHS 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

snoring may commence before the airway occludes, and apnea results Apneas/hypopneas terminate when the subject arouses, i.e., wakens

briefly, from sleep This arousal is sometimes too subtle to be seen on EEG but may be

detected by: cardiac acceleration, blood pressure elevation,

sympathetic tone increase arousal results in return of upper-airway dilating muscle tone

factors predisposing to OSAHS by narrowing pharynx include:

Obesity around 50% have a BMI >30 kg/m2 in western populations

shortening of the mandible and/or maxilla this change in jaw shape may be subtle and can be familial

Hypothyroidism Acromegaly predispose to OSAHS by narrowing

the upper airway with tissue infiltration male gender middle age (40–65 years) myotonic dystrophy Ehlers Danlos syndrome smoking

Epidemiology

frequency of OSAHS is in the range of 1–4% of the middle-aged male population

it is around half as common in women also occurs in childhood (usually associated with tonsil or

adenoid enlargement) syndrome also occurs in elderly, although frequency is

slightly lower in old age

Irregular breathing during sleep without daytime sleepiness is much more common

occurring in perhaps 1/4 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 daytime sleepiness impaired vigilance cognitive performance Driving Depression disturbed sleep Hypertension difficulty concentrating Unrefreshing nocturnal sleep nocturnal choking Nocturia decreased libido Daytime sleepiness may range from mild to irresistible sleep attacks can be indistinguishable from those in

narcolepsy sleepiness may result in inability to work effectively and

may damage interpersonal relationships 3 to 6 risk in accidents on the road or when operating

machinery

Cardiovascular and Cerebrovascular Events

OSAHS raises 24-h mean blood pressure 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 O2 desaturations / h 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

that this rise in blood pressure would increase risk of MI by around 20% and stroke by about 40%

observational studies suggest an increase in risk of MI and stroke in untreated OSAHS

studies suggest, but dont prove, increased vascular risk in normal subjects with raised apneas/hypopneas

Patients with recent stroke have a high frequency of apneas and hypopneas

seem largely to be a consequence, not a cause, of stroke and to decline over weeks after vascular event

There is no evidence that treating apneas/hypopneas improves stroke outcome

There has been debate for decades whether OSAHS is an adult form of sudden infant death syndrome

reported excess nocturnal deaths in subjects previously shown to have apneas/hypopneas

Diabetes Mellitus

association of OSAHS with DM 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

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/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 recovery period or as a consequence of sedation

Patients whose anesthesiologists have difficulty intubating are much more likely to have irregular breathing during sleep

referring patients suspected of having OSAHS for investigation

some elective operations may need to be postponed until the OSAHS is treated

Differential Diagnosis Insufficient sleepthis can usually be diagnosed by history Shift workthis is a major cause of sleepiness, especially in those over 40 years old

on either rotating shift or night shift work patterns Psychological/psychiatric causesdepression is a major cause of sleepiness Drugsboth stimulant and sedative drugs can produce sleepiness Narcolepsyaround 50 times less common than OSAHSnarcolepsy is usually evident from childhood or teens and is associated

with cataplexy Idiopathic hypersomnolencethis is an ill-defined condition typified by long sleep duration and

sleepiness Phase alteration syndromesboth 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

guideline I use for patients with troublesome sleepiness includes:

those with an Epworth Sleepiness Score >11 sleepiness during work sleepiness during driving poses problems ESS 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 ESS

patient and his/her partner often give divergent scores for patient's sleepiness, and in such cases higher of two scores should be used

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 . . .. . .. . .. . .. . .

Diagnosis obtaining a good sleep history from the patient and

partner asking both to complete sleep questionnaires Physical examination must include assessment of:

obesity, jaw structure, upper airway, blood pressure, predisposing causes (hypothyroidism and acromegaly)

Full polysomnographic or limited studies the diagnostic test must demonstrate recurrent

breathing pauses during sleep a reasonable approach at present is for patients with

troublesome sleepiness but negative limited studies to then have polysomnography to exclude or confirm

Obstructive Sleep Apnea Treatment

Whom to Treat ??????treatment improves symptoms, sleepiness, driving, cognition,

mood, QOL, blood pressure in patients who have: Epworth score of >11 troublesome sleepiness while driving or working AHI >15

for those with similar degrees of sleepiness and AHI 5–15, 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

treatment cannot be advocated for this large group: there is not evidence that treating nonsleepy subjects

improves their symptoms, function, blood pressure

Obstructive Sleep Apnea Treatment

How to Treat should have condition and its significance

explained to them and to their partner discussion of the implications of the local

regulations for driving weight loss reduction of alcohol consumption to reduce caloric intake alcohol acutely decreases upper-

airway dilating muscle tone Sedative drugs

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 to improve:

breathing during sleep, sleep quality, sleepiness, blood pressure, vigilance, cognition, driving ability, mood and

quality of life in patients with OSAHS finding the most comfortable mask from the ranges of

several manufacturers trying 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

pressure required to keep patient's airway patent 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 work by holding lower jaw & tongue

forward, thereby widening pharyngeal airway

MRSs have been shown to improve OSAHS patients' breathing during sleep, daytime somnolence, blood pressure

Surgery Four forms of surgery have a role in OSAHS

1) Bariatric surgery can be curative in the morbidly obese

2) Tonsillectomy can be highly effective in children but rarely in adults

3) Tracheostomy is curative but rarely used because of associated morbidity; nevertheless, it should not be overlooked in extremely advanced cases

4) 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

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

Choice of Treatment

CPAP and MRS are the two most widely used and best evidence-based therapies

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 there is evidence that CPAP improves driving, but there are

no such data on MRS CPAP is the current treatment of choice 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

Central Sleep Apnea 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

1) Hypercapnic CSA occurs in conjunction with diminished ventilatory drive in Ondine's curse (central alveolar hypoventilation)

2) Normocapnic 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

is relatively unusual in OSAHS

Daytime sleepiness may occur

Investigation

Identification of movement being particularly difficult in the very obese Many apneas previously labeled central because of absent thoracoabdominal movement are actually obstructive

CSA can only be identified with certainty if: 1) esophageal pressure or 2) respiratory muscle electromyography is recorded and shown to

be absent during the events

Central Sleep Apnea Treatment

Patients with underlying CHF 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

Positive Airway Pressure Therapy

Schellenberg, J ARRCCM 2000;162:740-748

Retrognathia in OSA