Anatomy

The pharynx is a funnel-shaped fibromuscular sac with a large upper portion and a narrow lower portion. This structure extends from the base of the skull to the esophagus at the level of the cervical vertebral bodies. 6th. On person mature, long wall posterior pharynx around 14 cm and this wall is the longest pharyngeal wall. The pharyngeal wall is formed by the mucosa, pharyngobasilar fascia, muscle sheaths, and part of the buccopharyngeal fascia. ^5,6

The muscles of the pharynx are arranged in circular and longitudinal layers. The circular muscles consist of the superior, middle, and inferior pharyngeal constrictor muscles. These muscles are located on the outside and are fan-shaped with each lower part covering part of the upper muscle from behind. On the anterior side, these muscles meet each other and posteriorly meet with connective tissue. Muscle action This constrictor is to narrow the lumen of the pharynx. This muscle is innervated by the vagus nerve. The muscles of the pharynx that arranged longitudinally consisting of m. stylopharyngeus and m. palatopharyngeus. These muscles are located on the inside. Musculus The stylopharyngeus functions to widen the pharynx and retract the larynx, while the palatopharyngeus muscle connects the oropharyngeal isthmus and raises the lower part of the pharynx and larynx. These two muscles work as elevators, the work of these two muscles is important when swallowing. Muscle stylopharyngeus innervated by nerve glossopharyngeus And

m. palatopharyngeus innervated by nerve vagus. ^5.6 Based on its location then the pharynx can be divided into the nasopharynx, oropharynx, and laryngopharynx. The nasopharynx is the superior part of the pharynx, which is bounded by the base of the skull superiorly, the soft palate inferiorly, the nasal cavity anteriorly, and the cervical vertebrae posteriorly. There are several important structures in the nasopharynx such as adenoids, lymphoid tissue on the lateral wall of the pharynx, the pharyngeal recess called the fossa of Rosenmuller , the torus tubarius, the choana, the jugular foramen through which the glossopharyngeal nerve, the vagus nerve, and the spinal accessory nerves of the cranial nerves, the internal jugular vein, the petrous part of the temporal bone, and the laceral foramen and the opening of the Eustachian tube. ^5,6

The oropharynx is also called the mesopharynx, because it is located between the nasopharynx and the laryngopharynx. This structure is bounded by the soft palate superiorly, the upper edge of the epiglottis inferiorly, the oral cavity anteriorly, and the cervical vertebrae posteriorly. The structures found in the oropharyngeal cavity are the posterior wall of the pharynx, palatine tonsils, tonsillar fossae, anterior and posterior pharyngeal arches, uvula, lingual tonsils, and foramen cecum. The oropharynx can be divided into two, namely the retropalatal region, which is the posterior border of the hard palate to the caudal border of the soft palate, and the retroglossal region, which is the caudal border of the soft palate to the base of the epiglottis. The laryngopharynx (hypopharynx) is the lowest part of the pharynx starting from the base of the tongue, the epiglottis superiorly, to the crocoid cartilage. ^5,6

Pharyngeal tonsils or adenoids are lobulated lymphoid masses consisting of from the network the same lymphoid as the there is on palatine tonsils. The lobes or segments are arranged in a regular manner as separate segments of a cavity with gaps or pockets between them. These lobes are arranged around a lower area in the middle, known as the pharyngeal bursa. Adenoids do not have crypts and are located in the nasopharynx on the superoposterior wall, although they can extend into the fossa of Rosenmuller and the orifice of the eustachian tube. The size of the adenoids varies from child to child. In general, adenoids will reach their maximum size between the ages of 3-7 years later will experience regression. ^5.6 Tonsils palatine is a mass lymphoid tissue Which located in in fossa tonsils on second corner oropharynx And bounded by the anterior pillar (m. palatoglossus) and the posterior pillar (m. palatopharyngeus). Tonsils are oval in shape with a length of 2-5 cm, each tonsil has 10-30 crypts that extend into the tonsil tissue. Tonsils does not always fill the entire tonsillar fossa, the empty area above it is known as the supratonsillar fossa. The tonsils are located lateral to the oropharynx, bounded by the superior pharyngeal constrictor m. on the lateral side, the palatoglossus m. on the anterior side, the palatopharyngeus m. on the posterior side, the soft palate on the superior side and the lingual tonsil on the inferior side. The surface of the palatine tonsils is covered with stratified epithelium flattened that also line the tonsillar invaginations or crypts. Numerous lymph nodes lie beneath the connective tissue and are scattered throughout the crypts. The lymph nodes are embedded in a stroma of reticular connective tissue and diffuse lymphatic tissue. Lymph nodes are an important part of the body's defense mechanism and are distributed throughout the body along the path of the lymphatic vessels. The nodules often coalesce and commonly show germinal centers. The palatine tonsils receive their blood supply from branches of the facial artery that enter the palatine tonsils at the inferior and forms branches of the tonsillar artery and palatine artery. ascending, besides also receiving blood flow from a. lingualis, a. pharyngeal ascending and a. pharyngeal descending branches of a. external carotid. The veins in the palatine tonsils are v. paratonsillar and end up forming the pharyngeal plexus. ^5,6

Definition

Obstructive Sleep Apnea Syndrome (OSAS) on child is condition apnea and/or hypopnea, which is the cessation of respiratory airflow for 10 seconds or more where there is a total or partial blockage. some airway obstruction that occurs repeatedly moment Sleep during non-REM (non-Rapid Eye Movement) or BRAKE (Rapid Eye Movement) causing airflow to the lungs to be blocked. This blockage causes the patient to wake up during sleep or there is a transition to an earlier stage of sleep. The term OSAS is used for total or partial airway obstruction syndrome that causes significant physiological disturbances with varying clinical impacts. The apnea-hypopnea index ( AHI) can be used as an indicator of the severity of OSAS 1,2,3

Prevalence

OSAS can occur at all ages including neonates . The prevalence of OSAS in child as big as 1–5 % And incidence highest happen between age 4-6 year (preschool age) because at this age tonsil and adenoid hypertrophy often occurs. In children, the incidence of OSAS is not related to gender, while in adults men are more common than women, which is around 3:1. Epidemiologically, OSAS is more common in adults than in children. ^2,4,5

Physiology Sleep

Sleep has REM and non-REM periods that change several times during sleep at night. This sleep development is related to the age and increasing size of the child (brain maturity), so the total amount of sleep required is reduced and followed by a decrease in the proportion of REM and non-REM. Non-REM sleep consists of 4 stages, namely: stage 1 occurs when feeling sleepy and starting to fall asleep. In stage 2, the EEG image observes waves with a frequency of 14-18 cycles per second, and this is called a sleep spindle . The period of stage 2 lasts from 10 to 40 minutes. Stages 3 and 4 are deep sleep stages, where people who are fast asleep are very relaxed because muscle tone disappears completely and the EEG observes slow delta waves (20-50%). Stage 4 is the deepest sleep, without dreams and difficult to wake up. At this stage, the breathing pattern and heart rate are regular and growth hormone is produced. ^7,8

REM sleep stage is very different from non-REM sleep. REM sleep is a very active stage of sleep. Breathing patterns and heart rate are irregular and there is rapid eye movement, hence the name REM sleep. Most of the limbs remain weak and relaxed. The sleep stage It is thought to play a role in finding and clearing thoughts, memory and maintaining the function of brain cells. ^7,8

During sleep, the opposite occurs, namely energy conservation, repair of body cells and growth. Because the concentration of adrenaline and cortisol decreases, the body begins to form growth hormones. In addition to playing a role in growth and development, this hormone also allows the body to repair and renew all body cells. This cell renewal process occurs faster than when awake. This is important evidence that sleep has an effect on children's growth and development. ^8,9

Pathophysiology

The pathophysiology of OSAS in children is not well understood, but it can occur if there is a disruption between the factors that maintain airway patency and the components of the upper airway that cause airway collapse. Obstruction in OSA is the result of impaired airflow caused by the collapsed pharyngeal wall. during sleep. The etiology and mechanisms of airway collapse are multifactorial but are associated with the interaction of a highly collapsible upper airway with relaxation of the pharyngeal dilator muscles that occurs during sleep. Obesity, hypertrophy of the pharyngeal tissue soft, craniofacial abnormalities such as retrognathia add to the tendency for obstruction by increasing intraluminal pressure in network around road breath above. But disturbance structural alone in the airway is not sufficient to cause OSA. Patients without anatomical abnormalities can also experience OSA, because the complex reflex pathways from the central nervous system to the pharynx that control the action of the pharyngeal dilator muscles fail to maintain pharyngeal patency. ^8,9

During sleep, the activity of the pharyngeal dilator muscles is relatively relaxed so that there is a tendency for the pharyngeal lumen to narrow during inspiration. In addition, nasal obstruction causes increased airflow resistance and worsens OSA. Obstruction nasal result in business breathing through mouth moment Sleep so that there is relaxation of the genioglossus muscle so that the tongue is shifted back. Snoring sounds arise due to turbulence of air flow in the upper airway due to obstruction. The location of the obstruction is usually at the base of the tongue or palate. Obstruction occurs due to the failure of the upper airway dilator muscles to stabilize the airway during sleep where the pharyngeal muscles relax, the tongue and palate fall back so that obstruction occurs. ^11,12,13

On child more often experience period obstruction partial road breath prolonged and hypoventilation than adults. The apnea state is more rarely on children and generally shorter time than in adults. Hypoxia and hypercapnia result from cycles of partial or complete obstruction. Obstructive apnea causes increased activity of the upper airway dilator muscles, resulting in termination of apnea. In children with OSAS, arousals are much less common, and partial obstruction may persist for hours without interruption. ^10,11

Factor predisposition

Predisposing factors for OSAS in children include adenoid and tonsil hypertrophy, craniofacial disproportion, obesity. Adenoid and tonsil hypertrophy are the most common conditions that cause OSAS in children. Although in most cases OSAS children improved after adenotonsillectomy, but a small proportion will persist after surgery. In children with craniofacial disproportion, it can cause airway obstruction even without adenoid hypertrophy, ^10,11

Another cause of OSAS is obesity. In adults, obesity is the main cause of OSAS, while in children, obesity is not the main cause. The mechanism of OSAS in obesity is due to narrowing of the upper respiratory tract due to the accumulation of fatty tissue in the muscles and soft tissues around the respiratory tract, as well as external compression of the neck and jaw. Determination of obesity can be done by calculating the index body mass (BMI) and circumference measurement neck. For determining OSAS, neck circumference plays a greater role than BMI. It is known that a large neck circumference or obesity in the upper area is associated with increased cardiovascular disease, and is also thought to be associated with snoring and OSAS. It is suspected that fat accumulation in the neck area can make the upper airway narrower. Another possibility is that obese patients with large necks have a velopharynx that is more prone to collapse, which can facilitate upper airway obstruction during sleep. ^10,11

Clinical Manifestations

The most common clinical manifestation is difficulty breathing during sleep which usually occurs slowly. Before symptoms of difficulty breathing occur, snoring is the initial symptom that appears. Snoring in children can happen continuously (every sleep) or just on certain positions only. A history of snoring more than 3 nights a week increases the suspicion of OSAS. In OSAS, children generally snore every time they sleep with loud snoring heard from outside the room and episodes of apnea are seen which may end with body movement or awakening (arrousal). Breathing efforts can be seen with retractions. The position when sleeping is usually prone, half Sit down, or hyperextension neck For maintain airway patency is sometimes found in children who sweat, are restless, often wake up, and have cyanosis. ^1,14

Pediatric sleep questionnaire

Considering that polysomnography is time consuming, expensive, and not necessarily available in health facilities, a method is needed. other methods as a screening test. The most widely used screening test is the pediatric sleep questionnaire which can predict whether a child is experiencing sleep-disordered breathing. This questionnaire consists of 22 questions that will be answered by the patient's parents. The answer choices for the questions include "yes", "no", or "Don't Know". The answer choice "Yes" is scored one point, the answer choice "no" is scored 0 points, and the answer "No" is scored 0 points. Know" issued from evaluation questionnaire. Questionnaire given score as: Score = (number of "yes" answers) : (total questions answered "yes" or "no"). Questionnaire score > 0.33 is considered a child at risk of experiencing sleep-disordered breathing. This scoring has a sensitivity value of 73% and a specificity of 83% compared to polysomnography. ^1,7,14

Observation during Sleep

OSAS events can be diagnosed by direct observation, the child told to sleep in the doctor's office or by reviewing audiotapes or videotapes that can be done at home. Some of the variables assessed are the hardness and type of inspiration, movement during sleep, frequency of awakening, number of apneas, retractions, and mouth breathing. Observation during sleep can be done using pulse oximetry. During sleep, the child is monitored for a decrease in saturation values using oximetry. Pulse oximetry recording in a way continuous during Sleep recommended as test screening and can show cyclic desaturation which is characteristic of OSAS, but cannot detect OSAS patients who are not related to hypoxia. If there is a decrease in saturation during sleep, then the possibility of suffering from OSAS is quite large, but if it is not detected on monitoring with oximetry, then a polysomnography examination is needed. ^1,7,10

Table 2. Friedman Classification ⁹

Lateral Positions

On radiography network soft neck can seen details network soft, This helps determine the anatomy of the upper airway and the size of the adenoids. A lateral plain radiograph of the neck can be used to determine the size of the adenoids. Although MRI can provide more detailed images of the soft tissues and bony structures underlying the nasopharynx, it is usually not necessary, except in cases of suspected anatomic abnormalities. ^1,7

MRI Head

Patients with a history of heavy snoring, headaches, neck pain, polyuria or swallowing problems should be suspected of having a Chiari malformation. This abnormality can occur in children with myelomeningocele. MRI is also performed in patients with suspected brainstem dysfunction. ^1,7

Management

Management of OSAS in children can be in the form of diet in children with obesity and use of CPAP (Continuous Positive Airway Pressure ), while the surgical procedures performed are tonsillectomy and/or adenoidectomy and correction of craniofacial disproportion. ^1,7

Lifestyle modification is necessary in obese patients, because weight loss body absolute done. With weight loss may lead to improvement of OSAS the real one. Unfortunately Losing weight in children is more difficult than in adults. In addition to improving diet in obesity, other diseases that may accompany it, such as diabetes mellitus, need to be considered. The ideal way is to lose weight slowly and consistently. This takes a long time, so counseling is needed for parents and children. ^5,6 Therefore, while waiting for weight loss, CPAP installation is needed. CPAP should be used until sufficient weight loss is achieved. In terms of obesity management, this includes behavioral modification, diet therapy, exercise , and medication. In patients with severe OSAS and potentially life-threatening complications, hospitalization is required. ^5,6 Children with OSAS will have clinical manifestations such as excessive daytime sleepiness. Therefore, restrictions on activities that require concentration need to be carried out. ^5,6

Medication Then become choice furthermore. Obstruction nose  is a factor that can generally facilitate the occurrence of OSAS in children, and can be treated with nasal decongestants or steroid inhalers. Nasal fluticasone given daily for 6 weeks has been shown to improve the frequency of obstructive events in children with mild to moderate. ^5,6

Nasal Continuous positive airway pressure or CPAP has been used with good results in children including infants, obese children, Down syndrome, achondroplasia, and craniofacial abnormalities. In the pediatric age group, CPAP is especially useful for obese patients and patients with OSAS that persists after tonsillectomy and/or adenoidectomy. The key to successful CPAP therapy is adherence to treatment and this requires good patient preparation, education, and intensive monitoring. The use of CPAP with a gradual increase in inspiratory pressure or with a lower expiratory pressure can improve patient comfort. ^12,13,14

Many experts believe that tonsillectomy and/or adenoidectomy are the actions that must be performed because the benefits are greater. The cure rate for this action in children is around 75-90%. In children with adenoid and tonsil hypertrophy etiology alone, the success rate is high, but if accompanied by other risks such as obesity and craniofacial disproportion, OSAS will still occur after surgery. However, because OSAS occurs due to the relatively small size of the upper respiratory tract component structure compared to the absolute size of the tonsils and adenoids, experts believe that tonsillectomy and/or adenoidectomy are still necessary in this situation. Post-tonsillectomy and/or adenoidectomy monitoring with polysomnography is required as a follow-up. Sometimes symptoms still persist and will disappear a few weeks later. Other medical management such as obesity management is still carried out even though tonsillectomy and/or adenoidectomy have been performed. ^10,11

Uvulopalatopharyngoplasty (UPPP) is not commonly performed in children. During the procedure, the uvula, posterior border of the soft palate, and lateral wall of the pharyngeal mucosa are removed using a scalpel or laser ablation. The success of UPPP surgery in reducing obstructive sleep apnea is only if the obstruction is localized to the soft palate. However, the risk after surgery is velopharyngeal insufficiency. Monitoring and polysomnography examination 2-3 months after surgery are needed to assess the success of therapy. ²Tracheostomy is a temporary measure in children with OSAS. severe life-threatening conditions and for children living in areas where surgical equipment is not available. ^11,13,14

Complications

Complications of OSAS occur due to chronic nocturnal hypoxia, acidosis, sleep fragmentation. This can cause neurobehavioral complications, failure to thrive, cardiovascular complications, enuresis, respiratory disease, respiratory failure to death. Neurobehavioral complications occur due to chronic nocturnal hypoxia and sleep fragmentation. Excessive daytime sleepiness has been reported in 31% - 84% of children with OSAS. Other complaints that can accompany OSAS are developmental delays, poor school performance, hyperactivity, aggressive / hyperactive attitudes, withdrawal from social life. Milder manifestations of cognitive impairment can often occur. A study showed that OSAS improvement can causes marked improvement in cognitive function. Failure to thrive is a common complication in children with OSAS approximately 27 - 56%. The causes of failure to thrive in children with OSAS are anorexia, dysphagia secondary to adenoid and tonsil hypertrophy, increased effort to breathe, and hypoxia. ^12,13,14

Repeated nocturnal hypoxia, hypercapnia and respiratory acidosis can result in pulmonary hypertension which is a cause of death. patient OSAS. Condition in on can develop become cor Pulmonary hypertension. The prevalence of pulmonary hypertension in children with OSAS is unknown. ^13,14

DISCUSSION

Clinical symptoms of OSAS in children that are worth investigating include increased breathing during sleep, bedwetting, sleeping in an abnormal position, frequent waking during sleep, morning headaches, hyperactivity, inattention, poor school performance decreased, feeling sleepy excessive, disturbance growth and weight. ^1.7

Currently, upper airway imaging is rarely performed to diagnose OSAS. In children suspected of having adenoid hypertrophy, a lateral head X-ray with soft tissue conditions can be performed. ^10,11

Inspection oximetry on Evening day aiming For identify patients who require polysomnography (PSG) examination. Oximetry examination is said quite sensitive though No quite specific in establish a diagnosis of OSAS. PSG examination is the gold standard in diagnosis of OSAS in adults and children. ^10,11 PSG examination also recorded sign physiological other such as an electroencephalogram (EEG), electrooculogram (EOG), electromyogram (EMG), air flow, oxygen saturation, respiratory effort, heart rate and electrocardiogram (ECG). ^10,11 The examination is carried out in the laboratory, the patient comes two hours before bedtime and has previously carried out daily activities as usual. PSG is recommended for patients who are at high risk for OSAS complications, such as patients with obesity, with heart disease, coronary artery disease or heart rhythm disorders. ^10,11 At the end of the PSG examination, the AHI calculation is carried out, which is used For determine degrees the weight OSAS, namely degrees light AHI 1- <5, moderate degree 5 - <10, And degree of severity > 10. ^10,11

OSAS therapy can be in the form of diet in children with obesity and the use of nasal CPAP (Continuous Positive Airway Pressure ), while the surgical procedures performed are tonsillectomy and/or adenoidectomy and correction of craniofacial disproportion. ^11,12,14

CONCLUSION

Obstructive sleep apnea syndrome is a syndrome with the discovery of apnea or hypopnea episodes during sleep. OSAS in children greatly affects the growth & development of children. Risk factors for OSAS in children include adenoid and tonsil hypertrophy, craniofacial disproportion and obesity. Complications that can occur are behavioral disorders, cardiovascular disorders, and failure to thrive. The definitive diagnosis of OSAS in children uses polysomnography, namely the presence of an apnea or hypopnea index of more than 1. Other supporting examinations are using a pediatric sleep questionnaire , video observation, using pulse oximetry.

Adenoid and tonsil hypertrophy are the most common causes of OSAS in children. The management of OSAS in children is adenoidectomy and/or tonsillectomy. The success rate is quite high, which is around 75%. In addition, diet for weight loss in obesity, as well as the use of CPAP (continuous positive airway pressure). It is expected with Handling Which appropriate And fast can reduce mortality rates and disability rates caused by OSAS.

REFERENCE

1. Mills. JH. Pediatric Sleep-Disorder Breathing. In Bailey, B.J.; Johnson, J.T.; Newlands, SD, editors. Head & Neck Surgery-Otolaryngology, Edition to- 4. Philadelphia : Lippincott Williams & Wilkins. 2006; 129:1080- 5.

2. Tran KD, Nguyen CD, Weedon J, Goldstein NA. Child behavior and quality of life in pediatric obstructive sleep apnea. Arch Otolaryngol Head Neck Swrg.2020;131(l):52-7.

3. Supriyatno B, Said M, Hermani B, Syarif DR, Sastroasmoro. Risk factors for obstructive sleep apnea syndrome in obese early adolescents: scoring system as diagnostic prediction, 2019.

4. 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; 2017; 250-261.

5. Rodriguez, Hector P. Berggren, Diana AV. Biology and treatment of Sleep Apnea. Otolaryngology chapter 6,2020; 71-82.

6. Mitchell RB. Adenotonsillectomy for obstructive sleep apnea in children: outcome evaluated by pre- and postoperative polysomnography. Laryngoscope . 2019; 117(10):1844-54.

7. Friedman M, Ibrahim H, Bass Lee. Clinical staging for sleep disordered breathing . Arch Otolaryngol. Head&Neck Surg . 2020: 13-21.

8. Schechter MS, Technical report: Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2021;109:1-20.

9. Newlands, Shawn D. Bailey, Biron J. Sleep Apnea-Assessment and Management of Obstructive Sleep Apnea in Adult .. Textbook of Head and Neck Surgery-Otolaryngology. 3rd edition. Volume 1. Lippincot: Williams & Wilkins. Philadelphia. 2005. 273-9.2000.

10. Smith RS, Ronald J, Delaive K, Walld R, Manfreda J, Kryger MH. What are obstructive sleep apnea patients being treated for prior to this diagnosis?. Chest 2019; 121:164-72.

11. Mitchell RB, Kelly J. Outcome of adenotonsillectomy for severe obstructive sleep apnea in children. Int J Pediatr Otorhinolaryngol . 2018; 68(11): 1375- 9.

12. Muntz H, Wilson M, Park A, Smith M, Grimmer JF. Sleep disordered breathing and obstructive sleep apnea in the cleft population. Laryngoscope. 2018;118(2):348-53.

13. Cohen SR, Ross DA, Lefarivre JF, Burstein FD, Riski J. Clinical practice guideline: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2019;109(4):704-12.