Transcript Dr.Samet.M Yazd University Harrison`s PRINCIPLES OF INTERNAL

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
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 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
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asymptomatic individuals with abnormal breathing during sleep should not be
labeled as having OSAHS
Clinical Indicators in the Sleepy Patient
Age of onset (years)
Cataplexy
OSAHS
Narcolepsy
IHS
35–60
10–30
10–30
No
Yes
No
Normal
Normal
Long
Occasional
Frequent
Rare
Yes, loud
Occasional
Occasional
Occasional
Occasional
Common
Usually few
Many
Few
Afternoon/evening
Afternoon/evening
Morning
<1 h
<1 h
>1 h
Night sleep
Duration
Awakenings
Snoring
Morning drunkenness
Daytime naps
Frequency
Time of day
Duration
Mechanism of Obstruction
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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:
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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
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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
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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
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daytime sleepiness
impaired vigilance
cognitive performance
Driving
Depression
disturbed sleep
Hypertension
difficulty concentrating
Unrefreshing nocturnal sleep
nocturnal choking
Nocturia
decreased libido
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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
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Cardiovascular and Cerebrovascular Events
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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
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Hepatic dysfunction has also been associated with irregular breathing during sleep
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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
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Differential Diagnosis
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
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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
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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
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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
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TOTAL
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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
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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
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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
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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
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Drugs
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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
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 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
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Health Resources
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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
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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)
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
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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
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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
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Positive Airway Pressure
Retrognathia in OSA
Schellenberg, J ARRCCM 2000;162:740-748