sleep apnea syndromes

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    Sleep Apnea Syndromes

    Introduction

    As you know nowadays there is a big interaction between dentistryand sleep positions to a

    point that now there is a specialty known as dental sleep medicine derived for the issue with

    an academy for it in the U.S. known as theAmerican academy of sleep medicine. Currently Im

    involved in a research with two of your master degree colleagues regarding the matter.

    Attention is needed here as patients who are represented with sleep apnea syndromes

    especially those who have obstructive sleep apnea, you as a dentist would be the first one to

    notice it and send him to a sleep evaluation.

    How much sleep and what is adequate?

    Now we all know that we approximately sleep about 1/3 of the daily 24hours which is on

    average about 8hours. Some people sleep more or less but for sleep to be refreshing or

    restorative i.e. adequate you need not only an adequate time of sleep but also an adequate

    depth and continuityof sleep (continuity means in one go and not fragmented also known as

    consolidated sleep).

    Stages of sleep

    Earlier adequate depth of sleep was mention and that meant we go through our sleeping

    process in stages. We have two generalized kinds of sleep the non-REM sleep and the REM

    sleep with REM standing for Rapid Eye Movement.

    In neurophysiology REM is known as an incense mental activity but complete muscleparalysis. Some researchers allocate it as being stage5 but it is commonly referred to as

    REM sleep

    Non-REM however is when the brain is resting but the patient is capable of moving andit is further subdivided into

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    o Light sleep Stage 1: 1-2.5% Stage 2: 45-55%

    o Deep sleep ( sleep) Stage 3: 3-8% Stage 4: 10-15% although there isnt that much of a difference between

    stages 3 and 4

    This histogram illustrates how we enter sleep and as you can see we travel from one stage into

    another. The blue bars represent the REM and during our movement between stages you can

    see the length of the REM increases as the night time gets closer to end i.e. at dawn/fajir and

    that is if you notice when most of your dreams occur; you dream immediately before waking

    up.

    There is a transition between wakefulness and sleep that is usually smooth which you arentable to feel. You can never pin point the exact moment you transitioned into sleep in unless

    you undergo a sleep study

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    Sleep Studies

    We call a sleep study a polysomnogram

    PSG and it is done over the entirety of a

    night (all night) in which we usually

    need the patient to sleep about 8 hours

    to score 1 record. Most people are not

    able to sleep for the entire 8 hours due

    to different reasons like not being

    comfortable using the pillow in the lab

    or the bed so sometimes half the

    wanted period of sleep is acceptable.

    When they have severe sleep

    deprivation is when they are able tosleep for the entire time.

    When we record a sleep study we divide

    up the inputs into 30sec intervals and

    we call these intervals epochs. The

    values we study from the polysomnography include

    EEG for the study ofbrain waves, EOG for the study ofeye movements thereby deciding whether it is a rapid eye

    movement REM or a slow eye movement,

    EMG which is either submental(on the chin) or on lower muscles (shoulders) as othersleep disorders can be associated with movement during sleep,

    EKG for the tracing of heart waves to record occurrences such as cardiac arrhythmias, measuring the oral and nasal airflow in which we could determine if the patient has an

    apnea or hypopnea,

    chest and abdominal respiratory effort through reading their movements to knowwhether it is an obstructive or a central disorder

    There are other things that we could include such as video monitoring and soundrecording the patient in the sleep lab to record behaviors and snoring.

    And these are the basics of the polysomnogram.

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    Apnea and Hypopnea

    Apnea is defined as the cessation of breathing airflowi.e. when you measure the airflow there

    is no tidal movementas in a straight line which lasts greater than 10 seconds.

    Hypopnea is defined as an incomplete cessation of breathing airflow causing a decrease in

    the amplitude of the wave by 50%. If its more than 50% then it is associated with a reduction

    of oxygenation.

    Now if I conduct a study on all of us in this hall I can find about 5-10% of us having a sleep

    apnea syndrome however the remaining 90-95% might have up to 5 apneas or a hypopneas

    during sleep which is at a normal rate but if the incidents exceed 5 times then the person is

    considered to have a sleep apnea syndrome and there are three types of sleep apnea

    syndromes:

    Obstructive apnea: here theproblem is centered on theupper airwayi.e. cessation

    of airflowat the nose and

    mouth with no problems

    arising from the CNS and

    chest and respiratory

    muscles are moving. OSA is

    a separate entity and has different etiologies and must be treated specifically.

    No waves > 10sec

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    Central apnea: here theproblem arises from the CNS

    where there is no respiratory

    effortin addition to the

    cessation of airflowi.e. nose

    and mouth obstructed and

    no movement in chest and

    abdomen therefore no tidal

    waves in the readings at all. In most cases this type of apnea can be associated with

    medical disorders such as strokes and heart failure and it often does not have a specific

    treatment. If possible we can only treat the disease that caused it but not treat the

    central apnea itself.

    Mixed apnea: here the apneamay start as obstructive andcontinue as central or vise-

    versa.

    In the past we used to have to ask the patient to sleep while an MRI is being conducted in

    order to see and prove an existing case of OSA but with the new advancements of the

    polysomnography we no longer need that technique. Also dude to the loud nature of an MRI

    machine the patient couldnt quite sleep through such noise therefore the entire process was

    an obsolete investigation.

    Apnea Hypopnea Index (AHI)

    When we study patients the values we note are called scores and this scoring is to count thenumber of apnea and hypopnea event. For example a patient who slept for 6 hours had 360

    apneas and hypopneas (we add the apneas and hypopneas scored together) recorded. We

    divide the recorded scoring by the number of hours slept

    events per hour. Now the

    scaling of the events is as fallows

    Normal: less than 5 events per hour Mild: 5-15 events per hour

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    Moderate: 16-30 events per hour Moderatelysevere: 31-39 events per hour Severe: over 40events per hour (believe it or not Ive seen cases with a 120 AHI)

    Pathogenesis

    The pathogenesis of the apnea-hypopnea is not yet clear as there are many theories such as

    functional abnormalities in the pharyngeal muscles which are augmented by the presence of

    some anatomic abnormality. Sometimes the sole pathogenetic mechanism is thepresence of

    an anatomical abnormalityand the biggest example is the obstructive sleep apnea OSA in

    children caused by tonsilar enlargement.

    So other examples regarding anatomical abnormalities/complications of OSA include nasal

    problems like

    Obesity being the biggest contributor chronic rhinitis with hypertrophy of the nasal mucosa nasal septum deviation nasal masses nasopharyngeal masses nasal polyps tonsilar and adenoid hypertrophy hypertrophy of congenitally low palate and uvula facial malformations chromosomal abnormalities such as down syndrome endocrine disorders such as hypothyroidism and acromegaly neurological and neuromuscular disorders such as post-poliomyelitis and muscle-

    dystrophy

    All these are examples of diseases of distorted craniofacial anatomy that may cause an airway

    obstruction.

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    Symptoms of OSA in adults

    A referral by a smart dentist is probably the most effective way for diagnosis because dentists

    receive all their patients open mouthed and most of the clues leading to OSA are seen in the

    oral cavity such as an enlarged uvula, a lowered palate, large tongue, large teeth, distorted

    teeth or micrognathia.

    Other symptoms include excessive day time sleepiness, snoring and witness apnea which is

    mostly alarming for a spouse as they witness the patient as theyve stopped breathing

    Finally non-specific symptoms include

    Restless sleep High blood pressure Morning headache Dry mouth upon awakening Depression Severe Anxiety Short term memory loss Intellectual deterioration Temperamental behavior Poor job performance Impotence

    To the right are all examples of a massive uvula, massive

    tonsils and a massive tongue that are all indications to an

    obstructive sleep apnea.

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    Above is whats known as the mallampati score which is used for OSA evaluation where the

    patients oral cavity is examined to see the rate of visibility of the tonsil, hard and soft palateand accordingly placed into one of 4 classes.

    A contributing factor to OSA is the neck size and BMI as the neck size is not only related to

    obesity as some patients with a normal BMI might have a thick neck which makes them

    exposed to OSA. If the neck size is over 16 inches and or the BMI is over 25 the person may at

    risk for an OSA.

    The reason were interested in

    studying OSA is because it contributes

    to mortality. To the left is a study

    conducted comparing mortality to

    apnea-hypopnea index and the fount

    that patients with anAHI above 20

    have a higher mortality rate than those

    with a AHI lower than 20.

    The mortality usually occurs fromcardiovascular events both heart and

    brain and traffic accidents as the driver

    can fall asleep causing an accident.

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    Further explanations

    What happens during sleep is that the entire body muscle system relaxes including the

    pharyngeal muscles so the opening of the pharynx reduces which is adequate for oxygenation

    as were not moving and dont need large amounts of oxygen.

    In OSA patients however they have an excessive narrowing of the pharynxto the degree which

    causes the snoring which progresses to the complete closure of the upper airwaywhich is the

    apnea itself. At this point the brain goes through a phenomenon known as anarousalwhich is

    sort of an alarming in the brain to send orders to the muscles to contract again upon which the

    muscles contract and the pharyngeal muscles contract resolving the apnea.

    This arousal is repetitive and with every arousal of the brain many systems in the body are

    stimulated such as the sympathetic system, the coagulated system, inflammatory pathways,

    metabolic deregulation and many, many more metabolic pathways are stimulated whicheventually leads to hypertension and ultimately both systemic and diastolic heart failure and

    many other cardiovascular events that lead to death.

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    Treatment Modalities of OSA

    Non-surgical treatmento Weight loss: a large amount of patients successfully reduce their AHI upon losing

    weight. If the patient cannot lose weight through diet and exercise then studies

    have shown that a gastric bypass surgery is helpful in both reducing the BMI and

    AHI

    o nCPAP: it is the gold standard treatment for OSA for patients who can tolerate theprocedure. It forms a pneumatic splint to the airway i.e. pushes through

    controlled air pressure that keeps the airway open as if its an air cast for the

    airway. The amount of pressure used is titrated in the lab so once we have the

    polysomnogram proving an OSA we readmit the patient into the sleep lab and

    apply the nCPAP and keep increasing the pressure until the polysomnogram

    comes out clean of an OSA reading. There are types of masks facial, oral or nasal

    depending on what the patient can tolerate. Some side effects include the fact

    that the patient has to exhale against the pressure provided by the machine. This

    helps in severe sleep apnea.

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    o Positional changes: during the polysomnogram taking there are sensors that letus know the position of the patient i.e. is he supine, lateral left or right and so on.

    If the OSA was recorded while the patient was supine then wed advice the

    patient to avoid sleeping in that position and as the movement during sleep is

    involuntary some tricks such as for patients who shave shown OSA in supine

    position to have a tennis ball placed in the back of their pajamas so that if they

    turn on their backs they would feel irritated and move to their side. As this is

    transitionalit helps in mild and moderate sleep apneas.

    o Orthodontic appliances: these are used incases of moderate to severe sleep apnea

    such as the equalizer, tongue retainers,

    mandibular advancing and mandibular

    repositioning appliances.

    Surgical treatmentso Uvulopalatopharygoplasty (UPPP)o Tracheotomyo Mandibular Advancemento Hyoid bone suspensiono Tonsillectomy & adenoidectomyo Thyroidectomyo Nasal septum deviation repair

    One of the most important things that you must keep an eye on especially as a dentist is if you

    suspect an OSA after taking the patient medical history that included clues such assnoring,

    excessive day time sleepiness,fat neckand so on you must warn him of using CNS depressants

    and alcohol within 4 to 6 hours of sleep and that he must warn the doctors if he is to have any

    operation as he is not allowed to be under any anestheticas these elements will prevent the

    brain from having arousals when its supposed to thereby killing the patient.

    Done by

    Mohamed Harun Sanoh

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