Transcript Obstructive apnea

OBSTRUCTIVE SLEEP APNEA
HYPOPNEA SYNDROME
BY
AHMAD YOUNES
PROFESSOR OF THORACIC MEDICINE
Mansoura Faculty of Medicine
According to the American
Academy of Sleep Medicine (AASM)
OSA is characterized by repetitive episodes of
complete (apnea) or partial (hypopnea) upper airway
obstruction occurring during sleep.
The 2007 AASM diagnostic criteria and definitions:-
• Apnea is defined as the drop in peak airflow by >90% of
baseline for 10 seconds or longer and at least 90% of the
event duration meet the amplitude reduction .
• Obstructive apnea is defined as contiued or increased
inspiratory effort throughout the entire period of
absent flow
• Mixed apneas ventilatory effort is not observed
initially (central apneic component), but ventilatory
effort follows (obstructive apnea component) .
The 2007 AASM diagnostic criteria and
definitions:• Hypopnea is defined as the drop in peak airflow by >30%
of baseline for 10 seconds or longer associated with
>4% desaturation from pre-event baseline and at
least 90% of the event duration meet the amplitude
reduction Or
• Hypopnea is defined as the drop in peak airflow by >50%
of baseline for 10 seconds or longer associated with
>3% desaturation from pre-event baseline or
arousal and at least 90% of the event duration meet
the amplitude
The 2007 AASM diagnostic criteria and
definitions:• Respiratory effort related arousals is defined as the
increase in respiratory effort or sustained respiratory effort
for 10 seconds or longer leading to arousal from sleep
when the sequence of breathes does not fulfil
criteria of apnea or hypopnea
• The criterion standard to measure RERAs is
esophageal manometry, as the AASM recommends.
However, esophageal manometry is uncomfortable
for patients and impractical to use in most sleep
centers.
Complex Sleep Apnea (CompSA)
CompSA consists of all or predominantly
obstructive apneas which convert to all or
predominantly central apneas when treated with a
CPAP or bilevel devices.
The RDI is defined as the number of obstructive
apneas, hypopneas, and respiratory event–related
arousals (RERAs) per hour. The RDI is preferred
over the AHI because it includes flow-limitation
events that end with arousals
The following criteria must apply for OSA to be diagnosed:
– The patient reports daytime sleepiness, unrefreshing sleep, fatigue,
insomnia, and/or unintentional sleep episodes during wakefulness.
The patient awakens with breath holding, gasping, or choking. The
patient's bed partner reports loud snoring, breathing interruptions, or
both during the patient's sleep.
– PSG shows more than 5 scoreable respiratory events (eg, apneas,
hypopneas, RERAs) per hour of sleep and/or evidence of respiratory
effort during all or a portion of each respiratory event.
– PSG shows more than 15 scoreable respiratory events (eg, apneas,
hypopneas, RERAs) per hour of sleep and/or evidence of respiratory
effort during all or a portion of each respiratory event.
– Another current sleep disorder, medical or neurologic disorder,
medication use, or substance use does not better account for the
patient's condition.
Historical perspectives
• In 1965, Gestaut, Tassinari, and Duron in France
and Jung and Kuhlo in Germany provided the first
accurate clinical descriptions of OSA at nearly the
same time.
• The first known successful treatment for OSA was
tracheostomy, which Elio Lugaresi and coworkers
first described in 1970 in Italy.
• For the next 11-16 years, tracheostomy was the
only established beneficial remedy for patients with
OSA.
• In 1981, Dr Colin Sullivan introduced continuous
positive airway pressure (CPAP) as a treatment for
OSA.
• In 1981, Fugita and colleagues introduced
uvulopalatopharyngoplasty (UPPP).
Frequency
• Although early investigators estimated the prevalence of
sleep-disordered breathing (SDB) to be 2% for middle-aged
women and 4% for middle-aged men, more recent research
indicates a prevalence of 4% for women and 9% for men.
• The National Commission on Sleep Disorders Research
estimated that minimal SDB (respiratory disturbance index
[RDI] >5) affects 7-18 million people in the United States and
that relatively severe cases (RDI >15) affect 1.8-4 million
people. The prevalence increases with age. OSA remains
undiagnosed in approximately 92% of affected women and
80% of affected men.
Pathophysiology
• pharyngeal collapse is responsible for the recurrent
UA obstruction during sleep in patients with OSA.
The retro-palatal area is the primary, but not only,
site of airway narrowing. Airway narrowing occurs in
ovoid geometric progression, with narrowing
occurring both laterally and antero-posteriorly.
• During wakefulness, the pharyngeal airway appears
to be smaller in patients with OSA compared with
healthy subjects. In the absence of craniofacial
abnormalities, the soft palate, tongue,
parapharyngeal fat pads, and lateral pharyngeal
walls are enlarged.
Diagnosis
• Clinical history and physical examination findings
are of paramount importance in the evaluation of a
patient with suspected OSA. Management
decisions should be made in the context of the
complete clinical picture because PSG evidence by
itself is insufficient to determine if a patient has
clinically significant OSA. Moreover, physical
findings alone cannot predict OSA.
Cardinal symptoms of sleep apnea
_ Loud, habitual snoring
– Apneic events witnessed or reported by spouses
or significant others
– Daytime sleepiness
• Predictive value
– Disrupted snoring: A history of disruptive snoring
has 71% sensitivity in predicting OSA
– Disruptive snoring and witnessed apneas: These
factors together have 94% specificity for OSA.
Other symptoms
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Non-restorative sleep
A choking sensation or gasping during the night
Morning headaches,
Insomnia
Restless sleep
Sore throat or dry mouth in the morning
Memory and intellectual impairment
Depression and anxiety
Impotence and decreased libido
Gastro-esophageal reflux disease
Physical EXAMINATION
• Obesity is a risk factor for OSA.
– 50% of patients with a BMI greater than 40 have OSA.
– Neck circumference may correlate with OSA better than
BMI.
– Women may have BMI lower than those of men.
– In women, the neck circumference is relatively normal
-UA abnormalities include severe nasal obstruction, lowhanging soft palate, large (hypertrophied) uvula, enlarged
tonsils and/or adenoids, and macroglossia.
• Systemic arterial hypertension is present in approximately
50% of patients with OSA.
• Craniofacial abnormalities
– Women may have a high, arched hard palate.
Structural factors
– Nasal obstruction that predispose patients with OSA to pharyngeal
collapse during sleep include polyps, septal deviation, tumors,
trauma, and stenosis.
– Retropalatal obstruction that predispose patients with OSA to
pharyngeal collapse during sleep include (1) an elongated,
posteriorly placed palate and uvula and (2) tonsil and adenoid
hypertrophy (particularly in children).
– Retroglossal obstruction that predispose patients with OSA to
pharyngeal collapse during sleep include macroglossia and tumors
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Genetic variations (facial elongation, posterior facial compression)
Retrognathia and micrognathia
Mandibular hypoplasia
Inferior displacement of the hyoid
Down syndrome
Marfan syndrome
High, arched palate (particularly in women)
Nonstructural risk factors
– Some nonstructural risk factors include obesity, age, male
sex, postmenopausal state, and habitual snoring with
daytime somnolence.
– Familial factors also play a role. Families with a high
incidence of OSA are reported. Relatives of patients with
SDB have a 2- to 4-fold increased risk of SDB compared
with control subjects.
– Environmental exposures include smoke, environmental
irritants or allergens, and alcohol and hypnotic-sedative
medications.
– Both hypothyroidism and acromegaly are associated with
macroglossia and increased soft tissue mass in the
pharyngeal region. They are associated with an increased
risk of SDB. Hypothyroidism is also associated with
myopathy that may contribute to UA dysfunction
Lab Studies
• Routine laboratory tests usually are not helpful
unless a specific indication is present.
• Consider obtaining a thyrotropin hormone level if
clinically indicated, particularly in elderly individuals.
• An arterial blood gas determination should be
obtained if obesity hypoventilation syndrome (or
another cause of clinically significant pulmonary
hypertension) is suspected.
Imaging Studies
• Modalities available for identifying the site of
obstruction include lateral cephalometry,
endoscopy, fluoroscopy, CT scanning, MRI.
• The accuracy of these methods in identifying the
sites of obstruction is not clear. At present, UA
imaging is used primarily as a research tool.
Routine radiographic imaging of the UA in the initial
evaluation of SDB patients is of uncertain benefit
and should not be performed unless a specific
indication is present.
The following PSG findings are
characteristic of OSA
• Apneic episodes occur in the presence of respiratory muscle
effort
• Apneic episodes lasting 10 seconds or longer are
considered clinically significant. Apneic episodes are usually
approximately 20-40 seconds and rarely last several
minutes.
• Apneic episodes are most prevalent during REM sleep.
• Mixed apneas may occur. Mixed apneas are a combination
of central sleep apnea and OSA in a single apneic episode.
• Sleep disruption due to arousals is usually seen at the
termination of an episode of apnea.
AASM guidelines for split-night PSG
studies
• Patients with an RDI of greater than 40 during the first 2
hours of diagnostic PSG should undergo a split-night PSG
study. The final portion of the study is used for titrating the
CPAP device. Split-night studies may be considered for
patients with an RDI of 20-40, as based on clinical
observations (eg, prolonged obstructive events, marked
oxygen de-saturation). A minimum of 3 hours of sleep is
preferred to adequately titrate the CPAP device after this
treatment is started.
A single split-night study may not permit adequate titration of
CPAP therapy. If treatment does not control symptoms,
additional full-night CPAP titration may be required.
Unattended PSG
• unattended portable PSG performed in the patient's
home may be effective for diagnosing severe OSA
when performed by a qualified sleep specialist as
part of a comprehensive sleep consultation.
Any patient who is initially tested with unattended
portable PSG studies and who does not have a
satisfactory diagnosis must have easy and
automatic access to a comprehensive sleep
consultation and additional diagnostic testing.
Limited PSG studies
• A portable monitoring device is being used for limitedchannel, in-laboratory diagnostic PSG studies
(cardiopulmonary monitoring). include assessments of oronasal airflow, chest-wall respiratory effort, ECG findings, and
oxy-hemoglobin saturation.
. Limited PSG studies may be indicated in the following
settings:
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Patients with severe symptoms indicative of OSA when
treatment is urgently needed and when standard PSG is not
readily available.
• Patients with established OSA who require follow-up
studies
• Patients who cannot be evaluated in the sleep laboratory
Repeat PSG
• Repeat PSG if symptoms persist despite adequate
compliance with prescribed CPAP treatment. PSG
can be used to assess response to UA surgical
procedures and to assess response to OA therapy.
If sustained weight change of greater than 15%
occurs, PSG should be repeated. Finally, if results
of the first PSG are of poor quality, a repeat study is
indicated.
Treatments
• All patients should be offered nasal CPAP therapy first.
• In patients with mild-to-severe OSA who refuse or reject
nasal CPAP therapy, BiPAP therapy should be tried next. If
this therapy fails or is rejected, OA therapy should be
considered.
• OAs may be considered first-line therapy for patients with
mild OSA, particularly if they are unwilling to try nasal CPAP
therapy.
• Patients in whom noninvasive medical therapy (eg, positive
airway pressure, OAs) fails should be offered surgical
options. Patients should be made aware of the success
rates for each surgical procedure. They should be informed
that they might require more than 1 surgical procedure,
some fairly extensive, to cure OSA.
General and behavioral measures
• weight loss and avoidance of alcohol use, sedative
use, and being in the supine position, are elements
of nonsurgical treatment.
• Pharmacologic therapy is not part of treatment.
• No clinically useful drug therapy is currently
available.
Guidelines for use of CPAP therapy
• Patients with (RDI >15) should be treated irrespective of
their symptoms because of the increased risk of
cardiovascular morbidity. Patients with an RDI of 5-15 should
be treated if they have symptoms or coexistent
cardiovascular disease.
• CPAP is titrated after the diagnostic portion of a split-night
protocol or on a separate night after a diagnostic PSG.
Proper titration includes identifying the minimum CPAP level
that abolishes obstructive apneas and/or hypopneas,
oxyhemoglobin desaturation, RERAs, and snoring in all
sleep stages and in all sleep positions. The pressure needed
is typically 5-20 cm of water.
BiPAP therapy
• No studies have conclusively demonstrated
improved compliance with BiPAP devices compared
with CPAP devices. In patients who cannot tolerate
CPAP, a trial of BiPAP is warranted. However,
BiPAP is too expensive to be used as first-line
therapy, and it has no distinct advantages over
CPAP therapy.
Treatment of snoring and OSA with OAs
• Although OA therapy is not as effective as CPAP, OAs are indicated for
use in patients with mild-to-moderate OSA who prefer OAs to CPAP,
those whose condition does not respond to CPAP, those who are not
appropriate candidates for CPAP, and those in whom attempted CPAP or
behavioral measures (eg, weight loss, changing sleeping positions) fail.
• Patients with severe OSA should receive an initial trial of nasal CPAP
because CPAP is more effective than OA therapy. UA surgery may also
supersede the use of OAs in patients for whom these operations are
predicted to be highly effective in treating sleep apnea.
• To ensure satisfactory therapeutic benefit from OAs, patients with OSA
should undergo PSG or an attended cardiorespiratory sleep study with
the OA in place after final adjustment of fit is performed.
• OAs have better success rates in patients with mild OSA (81%) than in
those with moderate (60%) or severe (25%) OSA.
Types of OA
• Ttongue-retaining device (TRD). incorporated a pliable bulb
in the front that holds the tongue forward. This bulb
prevented the tongue from collapsing back into the airway
during sleep.
• Mandibular re-positioners designed for mandibular
advancement. These repositioners are adjusted to advance
the jaw to 60-70% of the maximum protrusion of the jaw.
• Palatal lifting devices.
• More than 40 OAs are available to manage SRBD and
OSAS.
AASM recommendations for surgery
• Surgery is indicated in patients who have a specific
underlying abnormality that is causing the OSA.
• Surgery may be indicated if noninvasive medical
therapy (nasal CPAP or OA) fails or is rejected, if
the patient desires such therapy, and if he or she is
medically stable enough to undergo the procedure.
• If the patient has OSA that is moderately severe or
severe (RDI >40 or lowest oxy-hemoglobin
saturation <80%), the patient requires perioperative airway protection with either nasal CPAP
or a trache-ostomy.
Surgical procedures
• Functional division of the pharynx into retropalatal
and oropharyngeal and retro-lingual and hypopharyngeal regions has been proposed.
• Different surgical procedures have been proposed
for patients with different levels of obstruction.
UPPP may correct type I obstruction. Genioglossus
advancement with hyoid myo-tomy (GAHM) may
correct type III obstruction. Maxillo-mandibular
advancement osteo-tomy (MMO) may correct
obstruction at all levels.
Riley-Powell-Stanford surgical protocol
• Because several sites of obstruction may be
responsible, a systematic approach for selecting
surgery has been developed. This is the RileyPowell-Stanford surgical protocol designed in 1988.
The protocol has 2 phases.
• Phase I consists of the UPPP and GAHM
procedures,
• phase II consists of the more complicated MMO
procedure.
• Patients who are not adequately treated with phase
I surgery are offered phase II surgery.
Tracheostomy
• This procedure bypasses the UA and is the most
effective surgical procedure for treatment of OSA; it
is virtually 100% effective. Unfortunately,
tracheostomy is a disfiguring procedure and
decreases the patient's quality of life. Tracheostomy
is now reserved for patients with severe OSA in
whom other medical and surgical treatment
modalities fail. Tracheostomy is also used for airway
protection during UA reconstructive surgery.
Uvulo-palato-pharyngoplasty
• UPPP is the most common surgical
procedure performed for adults with OSA.
Fujita and colleagues introduced this
procedure to the United States in 1981.
UPPP involves removal of the tonsils (if
present), the uvula, the distal margin of the
soft palate, and the redundant pharyngeal
tissue, as well as reshaping of the soft
tissues in the lateral pharyngeal walls.
Uvulo-palato-pharyngoplasty
• complications can include the following:
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Pain with swallowing and pain with speech,
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Hemorrhage (2-4%)
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Swallowing difficulties, particularly regurgitation of food
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Long-term pharyngeal discomfort
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Disturbance in taste
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Numbness of tongue
• Nasopharyngeal stenosis
• Silent apnea may result. UPPP may end snoring but have
no notable effect on episodes of sleep-associated
obstruction. Patients must undergo postoperative PSG to
rule out persistent OSA.
Genioglossus advancement with hyoid
myotomy
• The genioglossus muscle is repositioned anteriorly
through an inferior mandibular osteotomy
(genioglossus advancement). This maneuver
places the pharyngeal muscles and the base of the
tongue on tension and expands the airway. The
hyoid is suspended to the superior edge of the
larynx and fixed in this position, adding to the effect
of genioglossus advancement.
Maxillo-mandibular advancement
osteo-tomy
• The mid-face, palate, and mandible are moved
forward in this procedure, increasing the space
behind the tongue and increasing tension on the
genio-glossus muscle. This surgery is more
extensive than any of the others described. It is
usually reserved for patients in whom other
treatment modalities fail.
Radiofrequency volumetric tissue reduction of the soft
palate (somnoplasty)
• A midline soft palate sub-mucosal scar is created by
using a needle electrode inserted near the border of
the hard palate and directing it toward the uvula.
Pulses of radiofrequency energy are delivered,
resulting in tissue necrosis and needle-tract fibrosis
over subsequent weeks to months.
Other surgical options
• Laser-assisted uvulo-palatoplasty is successful for reducing snoring in
90% of patients, but the success rate in patients with SDB is not clear. It
may cause more scarring than UPPP, and it could potentially worsen
apnea. Laser-assisted uvulo-palatoplasty is not recommended for the
treatment of OSA until further data are available.
• Laser midline glossectomy and lingualplasty are performed to enlarge
the retro-lingual region by using a laser to remove a portion of the
posterior aspect of the tongue. The role of these procedures in the
management of SDB has yet to be defined.
• Nasal surgery includes septoplasty, turbinectomy, and polypectomy and
may be useful as an adjunct to other procedures or to improve CPAP
compliance.
• Nasal surgery by itself is rarely effective for the treatment of OSA.
Drug Category: CNS stimulants
• May be used to promote daytime wakefulness in
sleep apnea patients who have residual daytime
sleepiness despite optimal use of CPAP. Modafanil
and armodafinil are indicated for OSA.