CHAPTER I

INTRODUCTION

1.1 Introduction
Sleep is a fundamental process that every human needs. Adult humans require an average
sleep 6-8 hours / day. Sleep consists of nonrapid eye movement sleep (NREM) and stage rapid
eye movement sleep stage (REM). More than half the total sleep is the NREM phase whereas 20-
35% is the REM phase. Sleep disorders often occur in the REM phase.1 The most common form
of sleep disorder is sleep apnea (stop breathing at bedtime), and the most common symptom of
sleep apnea is snoring.1,3
Snoring is a social and health problem. Snoring is a problem that disrupts the sleeping
partner, causing disruption to intercourse, decreased productivity, increased risk of traffic
accidents and increased health costs in OSA sufferers. Heavy snorers are more likely to suffer
from hypertension, stroke and heart disease than people who do not snore with the same age and
weight.1,3
According to existing studies, snoring and OSA increase the risk of hypertension two to
three times, as well as increasing the risk of doubling coronary disease or heart attack. Snoring
and OSA sufferers are also at risk of stroke two times higher than those not with OSA and
snoring.1
Snoring and OSA generally occur in adults, especially men, middle age, and obesity.
About 50 million Americans sleep snoring, and 20 million Americans suffer from sleep apnea
syndrome. It is responsible for increased complaints from couples and more importantly carries
an increased risk of cardiovascular disease and premature death

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 CHAPTER II
LITERATURE REVIEWS

2.1 Defenition
Obstructive Sleep Apnea (OSA) is a state of apnea (cessation of airflow for 10 seconds or
more resulting in 2-4% decrease in oxygen saturation) and hypopnea (reduction of air flow> 30%
for at least 10 seconds with oxyhemoglobin> 4% desaturation or reduction in air flow> 50% for
10 seconds with oxyhemoglobin desaturation> 3%) There is a total or partial blockage of the
airway that occurs repeatedly during sleep during non-REM or REM causing airflow to the lungs
to be inhibited. This blockage causes the patient to wake up during sleep or a transition to an
earlier stage of sleep
Obstructive Sleep Apnea is part of breathing stop syndrome. Sleep-stop syndrome is
divided into 3 types: the central type, the type of obstruction and the mixed type. In this type of
central air flow occurs due to the cessation of breathing efforts for a while because the brain
failed to send signals to the diaphragm and chest muscles to maintain the respiratory cycle.
While the type of obstruction occurs airflow resistance to the lungs.3,5,6
Snoring is an abnormal breathing mark that occurs due to partial obstruction so that the
incoming airflow will vibrate the molasses and surrounding soft tissues. This condition is
facilitated by the relaxation of the tongue, uvula and muscles in the upper airway. Obstruction
may occur partially (hypopnea) or total (apnea) .1,3

2.2 Epidemiology
OSA was first published in 1956 by Sidney Burwell, more than 50 years ago and his
clinical interests are now increasingly recognizable. The prevalence of OSA in developed
countries is estimated to reach 2-4% in men and 1-2% in women. Men are more likely to
experience OSA and often (but should not) also suffer from obesity. The prevalence of OSA in
men is 2-3 times higher than women. Not yet known why OSA is less commonly found in
women.1,3
The prevalence of OSA in children is about 3% with the highest frequency at the age of
2-5 years. The main causes of OSA in children are tonsil hypertrophy and adenoid, but can also

2
be due to craniofacial structural abnormalities such as Pierre Robin and Down syndrome. OSA
frequencies peaked in decades 5 and 6, and declined in the over 60s. But in general the OSA
frequency increases progressively with the addition of age 1, 2, 3
OSA is present in more than 40% of individuals with a BMK of 30 kg / m2 or individuals
with metabolic syndrome. Patients with cardiovascular disease had a high prevalence of OSA,
50% of patients with hypertension, 50% of patients with atrial fibrillation requiring cardioversion
measures, 33% of patients with atrial fibrillation alone, 33% of patients with coronary heart
disease, 50% of patients with acute stroke and 30-40% of patients with heart failure and systolic
dysfunction.1

2.3 Upper Respiratory Tract Anatomy

Figure 1: Upper respiratory tract

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2.4 Patophysiology
Obstruction in OSA is the result of a disruption of air flow caused by a collapsed pharynx
wall during sleep. Aetiology and multifactorial collapse mechanisms but are associated with an
extremely easy upper airway interaction with the relaxation of the pharyngeal muscle dilators
that occur during sleep. Obesity, soft-tissue hypertrophy, craniofacial abnormalities such as
retrognathia increase the tendency of collapse with increased intraluminal pressure in the tissues
around the upper airway. But structural disturbances alone in the airways are not sufficient
enough to cause OSA. Patients without anatomic abnormalities can suffer from OSA, this is
because the reflex pathway complex from the central nerve to the pharynx that guards the muscle
action of the pharyngeal dilator can fail to maintain the pharyngeal patency.1,3,7
At bedtime the muscle activity of the pharyngeal dilator is relatively depressed
(relaxation) so that there is a tendency of the narrowed pharynx lumen at the time of inspiration.
Why this happens only to some people, especially related to the size of the pharynx and the
factors that reduce the lumen static dimension so that it becomes narrower or closes at bedtime.
In addition, nasal obstruction causes increased airflow resistance and worsens OSA. Nasal
obstrusions that result in respiratory effort through the mouth during sleep so that occurs
genioglosus muscle relaxation as a result of the tongue shifted back.3
Snoring sounds arising from airflow turbulence in the upper airway due to blockage. The
site of occlusion is usually on the base of the tongue or palate. Blockage occurs due to failure of
the respiratory tract muscles to stabilize the airway at bedtime where the muscles of the pharynx
relax, the tongue and the palate fall backwards resulting in obstruction.3

Figure 2 : Partial and Total obstruction of upper respiratory tract

4
 Trauma to the upper airway tissue during snoring results in damage to the muscle fibers
and peripheral nerve fibers. As a result, the ability of the muscles to stabilize the airways is
disrupted and increases the tendency of the airways to experience obstruction. Obstruction that is
exacerbated by edema due to the vibrations that occur during snoring can contribute to the
progressiveness of snoring to sleep apnea in certain individuals.3
Obstructive Sleep Apnea (OSA) is characterized by recurrent collapse of the upper
respiratory tract either complete or partial during sleep. As a result, respiratory air flow is
reduced (hypopnea) or stalled (apnea) resulting in oxygen desaturation (hypoxemia) and patients
multiple times awake (arousal). Sometimes the sufferer actually awakens at the time of apnea
where they feel choked. More often the patient does not wake up but repeated partial arousal
occurs, resulting in reduced sleep or slow wave sleep. This situation causes sleepy sufferers
during the day, lack of attention, concentration and memory are disrupted. The combination of
hypoxemia and partial arousal accompanied by an increase in adrenergic activity causes
tachycardia and systemic hypertension. Many OSA sufferers do not feel that they have problems
with sleep and come to the doctor just because the sleeping buddy complains of a loud snoring
(pre-constructive phase) punctuated by a long-varied silent state (obstructive apnea phase) .3
Sleep consists of two phases of rapid eye movement (REM) or active sleep and non rapid
eye movement (NREM) or quiet sleep. In normal individuals the sleep cycle of NREM and REM
will occur alternately with REM sleep interval of 10-20 minutes every 90-120 minutes. REM
covering 25% of bedtime is characterized by rapid eye movement especially on
electrooculogram, loss of muscle tone and increased sympathetic activity (increased heart rate
and blood pressure). During REM sleep, respiratory control is often irregular, a brief episode of
apnea over 10-20 seconds is relatively common. At the NREM stage of minimal or no mental
activity, the respiratory-cardiovascular system is largely regulated by metabolic factors. NREM
sleep affects sympathetic activity, decreased heart rate, blood pressure gradually from level I to
lowest sympathetic activity at level IV.1
The main principle in OSA is the pushing of the tongue and the back of the palate until it
attaches to the posterior pharyngeal wall causing nasopharyngeal and oropharyngeal occlusion.
Sleep lying (supine) may cause airway collapse due to movement of the mandible, the mole's
palate and the tongue toward the back. Structural and functional factors play an important role in

5
determining the critical pressure of airway collapse. Narceptic narrowing due to micrognathia,
retrognathia, tonsillar hypertrophy, macroglosia and acromegaly may also increase the risk of
developing OSA. Central nervous system plays an important role in OSA combination of
decreased upper airway muscle activity during sleep along with small pharyngeal structures
forming critical pressure of upper airway collapse. The activation of chemoreceptors by
hypoxemia and hypercapnia during apnea results in hyperventilation with an unconscious
awakening process.1
In obese patients an increase in fatty deposits of the neck and parafaring space causes
constriction and compression of the upper respiratory tract and disrupts the dilator muscles that
maintain the patency of the upper respiratory tract. Obesity can reduce the volume of the lung
causing a reduction in functional residual capacity. Changes in lung volume significantly
decreased the size of the upper respiratory pharynge through the mechanical effects of tracheal
and thoracic traction known as 'tracheal tug' increased the risk of collapse.7

2.5 Clinical Features

that can be found in OSA sufferers are snoring, excessive sleepiness during the day,
choking on sleep, apnea, nocturia, morning headaches, decreased libido to impotence and
enuresis, irritability, depression, extreme fatigue and insomnia. Most people complain of
drowsiness that is very disturbing during the day, causing problems in the association,
occupation and increase the risk of traffic accidents.1,2,3
OSA sufferers often also suffer from obesity. Awareness of a relationship between OSA
and obesity is very high can reduce awareness of the possibility of OSA in people who are not fat
(non-obese). Only about 50% of patients diagnosed with OSA also suffer from obesity.2

2.6 Diagnoses
Many OSA sufferers do not feel that they have problems with sleep and come to the
doctor just because the sleeping partner complains of a loud snoring sound (pre-obstructive
phase) interspersed by varying length of silence (obstructive apnea phase) .1,3,6
The Epworth sleepiness scale is used to assess sleepiness in the afternoon. OSA was
suspected in patients with scores above .2.7

6
 Situation 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 a lunch without alcohol ____________

In a car, while stopped for a few minutes in traffic

______

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 Epworth sleepiness scale

0 = no chance of dozing

1 = slight chance of dozing

2 = moderate chance of dozing

3 = high chance of dozing

The measurement of BMI, blood pressure, and neck circumference is an important

parameter in the OSA examination parameters. From the physical examination should be
identified the position and size of the maxilla and mandible bone and facial characteristics
should also be identified.7
Physical examination is performed on the nose, oropharynx, hypopharyngeal, larynx, neck to
determine the presence of obstruction in the section:
i. Nose: septum deviation, adenoid hypertrophy, tumor or nasal polyp, konka hypertrophy
ii. Oropharynx: large molasses, hypertrophy tonsil palatine, macroglosia, thickening (appeal)
of the posterior wall of the pharynx
iii. Hypopharyngeal: Collapse of lateral pharyngeal wall, hypopharyngeal tumor, lingual
tonsil hypertrophy, retrognathia and micrognathia
iv. Larynx: paralysis of the vocal cords, laryngeal tumors
v. Neck: measure the girth
Fiberoptic nasopharyngoscopy is a technique used for the evaluation of airway. This tool
is important for the identification of the site and location of obstruction: nasal, retropalatal or
retrolingual. Muller maneuver goodness and limitation were also used for examination for
preoperative prediction of effectiveness of surgical intervention based on several studies
conducted.
Muller maneuvers are performed in conscious patients who produce negative pressure by
inhalation / inspiration by closing the mouth and nose that will cause collapse of the breath.7
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 Cephalometric radiograph - 2-dimensional image generated member bone and soft tissue
skeletal information. this may confirm OSA patients through bone displacement of the hyoid to
the inferior, narrow posterior air space, longer molle palate than non-OSA.7 patients
Definitive diagnosis of OSA and CSA patients with polysomnographic examination.
Polysomnography is a standard Gold examination for diagnosis of OSA. In OSA to see episodes
of recurrent airflow followed by continuous respiratory effort whereas in CSA to see recurrent
episodes of apnea followed by loss of ventilation effort, breathing movements are halted due to
loss of movement of the ribs and abdomen as well as diaphragm electromyography activity.
Polysomnography is a diagnostic test tool evaluating sleep disorders, performed at night in sleep
laboratories. Examination consists of electroencephalogram (EEG), electromyogram (EMG),
electrooculogram (EOG), respiratory parameters, electrocardiogram (ECG), oxygen saturation
and microphone to record snoring. Patients are monitored for 6 hours 10 minutes.5
OSA screening can be done with a Berlin questionnaire that aims to capture patients to
OSA. This questionnaire consists of 3 parts: the first part contains about whether they snore,
how hard, how often and whether to disturb others. The second part is about exhaustion after
sleep, how often to feel tired and never fall asleep while driving. The third section contains a
history of hypertension, weight, height, age, gender and Body Mass Index (BMI). A person is
considered to be at high risk of OSA if it meets at least 2 of the above criteria. This
questionnaire has a high validity.3.5
The weight category of sleep apnea based on AHI consists of mild sleep apnea with AHI
5-15, 86% oxygen saturation and mild complaints, moderate sleep apnea with AHI 15-30, 80-
85% oxygen saturation and drowsiness and difficulty of concentration, severe sleep apnea with
AHI 30, oxygen saturation less than 80% and sleep disturbances.5

2.7 Treatment
A. Non-surgical therapy
therapy undergoes a revolutionary change when Sullivan et al. introducing the
Continuous Positive Airway Pressure (nCPAP) nasal. The principle of nCPAP is very simple,
that is, by giving positive pressure through the nose, any tendency of the airway to narrow and
close can be overcome and the airway wall can be stabilized so as to suppress snoring sound,

9
normalize the quality of sleep and relieve symptoms during the day. The effectiveness of
treatment in this way reaches 90-95% .3,6 In addition, Bi-level PAP is a noninvasive respiration
device that provides different inspiratory pressure (IPAP) and expiratory (EPAP) to
spontaneously breathing patients to maintain airway top remains open. By passing a low pressure
during the expiratory phase, the total pressure present in the airway can then be lowered to close
to normal breathing. Bi-levels have an additional flow to get the desired ventilation in patients
with various respiratory problems and have been used in OSA therapy. The advantage of this
method is to decrease the work of breathing
CPAP is a technique often used in non surgical management of OSA and is the treatment
of OSA's first therapy. CPAP reduces snoring and apnea and improves the symptoms of
oversleeping by noon. American college of Chest Physicians recommend the use of CPAP in
patients with RDI> 30 times / hour and to all symptomatic patients with RDI 5-30 times / hour.
CPAP 90-95% effective in OSA elimination and its effectiveness lies in the compliance and
regularity of patient use.8
In patients with obesity is recommended obesity weight loss. It needs to do lifestyle
changes including diet, exercise, and medical. Based on the study, weight loss 10% - 15% was
associated with a 50% decrease in apnea incidence and clinical improvement. Some case reports
show symptoms of OSA can be overcome by reducing weight. Sleeping position can help relieve
symptoms of OSA. Some patients experience improvement after sleeping on their side or prone
(pronation) .5
One of the newest treatment approaches is the use of mandibular advancement tools with
some variations. It is attached to the tooth and holds the mandible and tongue forward (partial
protrusion of the lower jaw) so as to maximize pharyngeal diameter and reduce the likelihood of
collapse during sleep. This tool is only used in patients with OSA who can not undergo surgery
and patients with mild to moderate OSA especially those who are not overweight or in patients
who are intolerant of CPAP. But keep in mind this tool can affect the occlusion and
temporomandibular joints so that its use is needed an orthodontic because the manufacture
depends on the individual.3

B. Surgical Therapy

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 Some patients can not receive treatment with nCPAP for several reasons, including
claustrophobia, noise from the engine and due to side effects such as nasal congestion and nasal
mucosa and dry mouth. Many patients do not want to use CPAP tools because they are
uncomfortable and reduce aesthetic value, so that other forms of OSA.3,5
Surgical treatment may be performed in a specific anatomic region causing airway obstruction in
accordance with sleep endoscopy examination results. Several operating procedures can be
performed:
1. Tonsillectomy and adenoidectomy. In patients with OSA with large tonsils, tonsillectomy
can relieve symptoms completely and does not require CPAP therapy.6
2. Uvulopalatofaringoplasti (UPPP). This method of uvula and excessive pharyngeal tissue is
removed so that the pharyngeal space increases as well as rigid the pharyngeal wall which will
prevent collapse. This method has a 50% success rate in curing OSA. Complications of this
method is the occurrence of nasopharyngeal regurgitation at drinking but only temporary
because it will decrease in 3 months.3
3. Surgery in the nasal area such as septoplasti, functional endoscopic sinus surgery and
concotomy can be an effective therapy when a blockage occurs in the nose. Nose
abnormalities should be sought in patients who experience nasal symptoms in treatment with
CPAP.4
4. Laser-Assisted Uvulopalatoplasty. Technique used by most surgeons removing parts of the
network triangle adjacent to each side of the root of the uvula followed with a 50% reduction
of the distal uvula thus shortening and increase the size and position of uvulopalatal
complex.3,6
5. Maxillofacial (Skeletal) Surgery. This technique increases the size of the upper airway by
moving the base of the tongue away from the posterior hypopharyngeal and oropharyngeal
wall, decreasing collapsed airway. Patients were selected based on their severity of apnea
(moderate to severe), craniofacial abnormalities, such as micrognathia or retrognathia, or
failure to respond to other therapies.3,6
6. Radiofrequency Tissue Volume Reduction. This technique incorporates electrodes to
various parts of the soft palate and apply heat energy, soft tissues will experience
'Thermal lesions will result in tissue fibrosis. this procedure can be repeated several times and
in some site targets of the upper airway, including tonsils and tongue base.3,6

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 7. Installation of Pillar implants on the palate. `Pillar implants or palatal implants are a
relatively new technique, a modality with minimal invasion. Used for patients with habitual
snoring and mild to moderate OSA. This procedure aims to give stiffness to the mole palate.
Three small rods are inserted into the mole's palate to help reduce the vibrations that cause
snoring
8. Tracheostomy- the surgical treatment of the gold standard and last if other methods do not
work is tracheostomy. Tracheostomy is performed by by pass obstruction of the upper
respiratory tract. Indications of tracheostomy are patients with cor pulmunale, obesity
hypoventilation syndrome, arrhythmias, CPAP-intolerant patients and other surgical
interventions.8

TP is highly sensitive to penicillin. It acts by interfering with the bacterial cell wall

2.8 Prognosis
OSA can have an impact on many systems of the human body, including: 1-5
1. Neuropsychological: excessive sleepiness during the day, lack of concentration and
memory, headache, depression.

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 2. Cardiovascular: tachycardia, hypertension, arrhythmia, heart blockade, angina,
ischemic heart disease, congestive heart failure, stroke.
3. Respiration: pulmonum hypertension, cast pulmunale.
4. Metabolic: diabetes, obesity.
5. Genito-urinary: nocturia, enuresis, impotence.
6. Hematologis: polycythemia.
From epidemiologic studies it is known that there is a relationship between OSA with
hypertension, stroke and ischemic heart disease. The incidence of cardiovascular disease in
patients with OSA is suspected as a result of repeated sympathetic stimulation that occurs at the
end of each obstructive phase. In patients with OSA also occurs the release of prothrombin and
proinflammatory factors that play an important role in the occurrence of atherosclerosis.1
The occurrence of cardiovascular disorders in patients with OSA is estimated through
two components: 1.3
1. Mechanical effects of breath stops on intrathoracic pressure and heart function.
2. Hypoxemia that occurs repeatedly leads to excessive sympathetic stimulation and
dysfunction of endothelial cells.
Approximately 40% of people with OSA develop hypertension when they wake up. OSA
is known as an independent risk factor for hypertension. How OSA causes elevated blood
pressure is not yet fully known. There is a potential role of sympathetic hyperactivity in elevated
blood pressure in OSA patients. Other mechanisms that potentially increase blood pressure in
patients with OSA are hyperleptinemia, insulin resistance, elevated levels of angiotensin II and
aldosterone, endothelial cell dysfunction, and impaired barorefleks.1
OSA is thought to be an independent risk factor for the occurrence of atherosclerotic
disease in arterial blood vessels. Many researchers have suggested several possible mechanisms
of atherosclerotic effects of OSA, including: Increased recurrent blood pressure due to
sympathetic hyperactivity and oxidative stress. Endothelial cell dysfunction resulting in elevated
plasma endothelin levels, decreased nitric oxide production, and increased inflammatory
response is evidenced by increased levels of C-reactive protein and interleukin-6.
Several studies have suggested a possible link between OSA and myocardial infarction.
The mechanism may be through the indirect effects of hypertension, atherosclerosis, oxygen

13
desaturation, sympathetic nervous system hyperactivity, increased coagulopathy and
inflammatory response.1,3
The incidence of high OSA (45-90%) is found in stroke patients. The possible role of
OSA in the pathogenesis of stroke is through the process of atherosclerosis, hypertension,
decreased cerebral perfusion due to thickening of the carotid artery wall, low cardiac output,
elevation of intracranial pressure, increased coagulopathy and increased risk of blood clot
formation due to arrhythmia. Due to the high incidence of OSA and its potential effects on
morbidity and mortality, checks for diagnosing and treating OSA are recommended for stroke
patients.1
Arrhythmia can occur in OSA patients, especially sinus bradycardia, sinus arrest, and
complete cardiac blockade. The risk for the occurrence of arrhythmias is related to the severity of
OSA. The mechanism of the occurrence of arrhythmia in patients with OSA is likely through
increased vagus tonus mediated by chemoreceptors due to apnea and hypoxaemia.

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 CHAPTER III
CONCLUSION

Obstructive sleep apnea is a sleep disorder that means stop breathing during sleep with
the main symptoms of snoring. OSA occurs because the tongue and palate fall backwards so that
obstruction occurs. Symptoms of OSA are snoring, excessive drowsiness during the day, choking
on sleep, apnea, nocturia, headaches in the morning. The diagnosis of OSA is best classified
according to the American Academy of Sleep Medicine. Complications of OSA are
hypertension, heart attack and stroke. OSA therapy is non-surgical therapy and surgical therapy.

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 REFERENCES

1. Febriani, Debi dkk. Hubungan Obstructive Sleep Apnea Dengan Kardiovaskular. Jurnal
Kardiologi Indonesia 2011; 32:45-52.
2. Committee Advisory, 2005. Sleep Apnea-Assesment and Management of Obstructive Sleep
Apnea in Adult.
3. Rodriguez, Hector P. Berggren, Diana A-V. Biology and treatment of Sleep Apnea.
Otolaryngology chapter 6, 2006; 71-82.
4. Hormann, Karl. Verse, Thomas. Sleep Disordered Breathing. Surgery for Sleep Disordered
Breathing. 2005; 1-10.
5. Antariksa, Budhi. Patogenesis, Diagnosti dan Patogenesis OSA (Obstructive sleep Apnea).
Dept pulmonologi dan Respirasi. FKUI. Jakarta.
6. Prasenohadi. Penatalaksanaan Obstructive Sleep Apnea. Dept Pulmunologi dan Respirasi.
FKUI. Jakarta.
7. Paul W. Flint, Bruce H. Haughey, Valerie J. Lund, John K. Niparko, Mark A. Richardson,
K. Thomas Robbins, J. Regan Thomas, Cummings Otolaryngology Head and Neck Surgery
5th Edition, Chapter 18: Sleep Apnea and Sleep Disorders ; 250-261.
8. Anil K Lalwani, Current Diagnosis & Treatment in Otolaryngology Head and Neck Surgery
2nd Edition, Lange Current Series, 536-542

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