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Sleep Apnea OBTURKTIVE IN CHILDREN

 Sleep Apnea OBTURKTIVE IN CHILDREN

By:
Tutut SRIWILUDJENG T.
Dr. Wahidin Sudiro Husodo Mojokerto

1. PENDHULUANObtruktive sleep apnea in children is a breathing disorder during sleep characterized by obtruksi partial upper airway and / or obtruksi entire airway is intermittent (obtruksi apnea) which menggaggu normal ventilation during sleep and interfere with normal sleep patterns. OSA in children associated with habitual snoring, sleep difficulties, and problems neurobehavial.OSA in children by Guilleminault siperkenalkan first time in 1979. OSA are common but often undiagnosed. The situation can be menyababkan morbidity if not detected and treated appropriately. Complications are often terjad include growth disorders and neurological disorders.OSA can about the child and adult. The prevalence of OSA in children around 1-5% with most cases found in babies of women. OSA is found at the age of 2-5 years with the highest incidence in the black and Hispanic. Boys - men more affected than women.OSA in children - children are different from adult OSA, especially in terms of clinical manifestation, diagnosis and therapy. Clinical symptoms of OSA is a decrease in air flow (Hypopnea) or cessation (apnea) of oronasal airflow. OSA is a disorder that includes a soft purr to prolonged episodes of nocturnal apnea. Currently onernight polysomnography used as a tool for diagnosing OSA in children. Photos lateral neck can be used to determine the existence of adenoid enlargement ..OSA Therapy consists of surgical therapy and non-surgical. In general, non-surgical therapy is limited in patients with OSA children. Surgical therapy consists of tonsillectomy and / or adenoidektomi in OSA cases that do not improve after tonsillectomy and adenoidektomi.
2. Sleep Apnea OBTRUCTIVE IN CHILDREN2.1 DefinitionOSA (Obtructive Sleep Apnoea) in children is defined as a respiratory disorder during sleep characterized by the presence obtruksi partial upper airway and / or obtruksi entire airway is intermittent (obtructtive apnea) that disrupt ventilation during sleep and interfere with normal sleep patterns.
2.2 EtiologyObtruksi on nasal airway pharing and played a role in the occurrence of OSA. OSA commonly found in children with developmental delay, neurological disorders and Craniofacial dismorfirm. In children with Down syndrome, makroglosi be the cause of OSA.The cause of OSA can be divided into the cause of local or systemic disease or other syndromes.Table 1. local cause of obstructive sleep apnea in childrenOropharyngeal Nasal / nasopharyngealEnlarged tonsilsRetrognatiaMakroglosiaGlossoptosis RhinitisAdenoid hypertrophySeptal deviationMassa on nasopharing
Table 2. disease and the syndrome causes of obstructive sleep apnea in childrenDisease syndromeCerebral palsyReticulosisSickle cell diseaseaAchondroplasiaObesityMukopolisakaridosisOsteopetrosisHypothyroid Down syndromeCrouzon syndromePreder-Willi syndromeApert syndromeTeacher-Collins syndromePierre-Robin syndromeKlippel-Feil syndrome

2.3 Pathophysiology of OSAPathophysiology of upper airway obstruction in infants and children - children are complex and not fully understood. Airway in children more susceptible to the occurrence of obstruction due to a smaller size and decreased muscle tone and a high larynx position. OSA occurs when the upper airway collapse in during respiration. The most easily collapse is at the entrance to the larynx and folds eryepiglotis. Muscle tone around pharing role in preventing airway collapse during neck flexion.During the process of inspiration. M.geniohyoid m.genioglossudan contraction of the tongue also widen the upper airway and making it resistant to collapse by negative pressure.Pharing airway depends on the dynamic balance between the strength of contraction of the diaphragm, upper airway resistance and strength of muscle contraction - muscle dilators.Sleep is a predisposing factor for the occurrence of airway obstruction. This is expected because the decrease in muscle activity during REM sleep, especially during the phase. Waking is a stimulator effect on airway dilators muscle and is responsible for the termination of spontaneous episodes of obstructive apnea.Drugs - drugs such as alcohol, sedatives and narcotics as well as lesions of the brain stem, play a role in the occurrence of OSA by pressing the airway defense activities.The main factor causing OSA in children - children are a prominent lymphoid tissue where the increase of airway resistive load. Refinements pharing as found in various craniofacial syndromes can place the tongue backward and cause obtruksi. Diseases - neuromuscular disease can cause muscle hipotonia pharing.Obesity increases resistance and lower compliance pharing thorax. Flexion of the neck is also a predisposing the occurrence of airway obstruction. Family can be a predisposing factor for a child suffering from OSA to affect airway resistive load through a craniofacial abnormality or dysfunction and ventilation control. More research is needed to examine the influence of family factors in OSA and other pathophysiological mechanisms.
2.4 Clinical manifestationsIn children, clinical symptoms that arise are non-specific and require special attention from parents or caregivers.Common symptoms of the most common is the child snore loudly and breathing difficulties during sleep.Unusual sleep position is where the child snore with neck extension or prone position with knees folded under the abdomen to eliminate obtruksi airway. Headache when you wake up, all day fatigue, night sweats, drolling, impaired growth and impaired weight gain, child behavior problems in some children found decreased school achievement. A history of loud snoring 3 nights or more per week should raise suspicions against the occurrence of OSA in children. OSA in children is characterized by breathing through the mouth while the child is either sleeping or during activities.Family history of snoring, allergies, and exposure to cigarette smoke is closely associated with the onset of snoring sound during sleep in children - children.
2.5 Physical ExaminationOn physical examination is often obtained hypertrophic tonsils and or adenoids, breathing through your nose and pectus excavatum. Careful examination is required to seek mucosal edema, cobblestone pattern of the mucosa, polyps, and decrease in nasal airflow. The evaluation of the position and size of the tonsils and uvula, especially to see the existence of hypertrophy and malformations. Although tonsil hypertrophy contribute to the severity of OSA, but few data are available are not able to explain clearly the relationship between the size of tonsils with and the frequency or severity of episodes apneu. Hypertrophy of tonsils, although many are found in patients with OSA, but as much as 57% are also found in healthy children without OSA.Mallampati classification is used to distinguish the degree of oropharyngeal obstruction. This classification is based on anatomical steruktur apparent when patients are meksimal open mouth with tongue removed.Class 1: soft palate and uvula visible MolleClass 2: Molle palate and uvula visible partClass 3: Molle palate and base of uvula visibleClass 4: Only hard palate visible
2.6 Diagnosis of OSASnoring is a clinical manifestation of airway obstruction, the condition can occur alone (primary Snoring) or associated with hipopnea, apnea or as part of the OSA. Airway obstruction during sleep in children are common, but some circumstances it can not meet the criteria of OSA.Diagnosis of OSA in children properly is not easy because the variation of normal sleep patterns that differ according to age in children. Lack of measurement methods available which can sleep apnea, especially in premature infants is a physiological state, but in school-age children is pathological.American Academy of Pediatrics, Pediatric subcommite obstrukstive sleep apnea syndrome in 2002 using the method of clinical assessement score, polysomnogrphy (PSG) and pulse oxymetri for diagnosing OSA in children.Table 1. Clinical Assessement Score

The frequency or severity of clinical and physical examination (Score)


Clinical
Frekuensi atau keparahan dan pemeriksaan fisik (Skor)
Every night

4-6 weeks/mgg

1-3 night/mgg

never
Symptoms night




Snoring
6
4
2
0
Stop breathing
6
4
2
0
The duration of stoppage of breath
6 (>15 secon)
3 (5-15 secon)
2 (0-5 secon)
0
movement whith chest
6
4
2
0
Gasping
6
4
2
0
Choke
3
2
1
0
Night sweats
3
2
1
0
Frequency woke up
3
2
1
0
Enuresis
6
4
2
0
Extended Neck
6
4
2
0
Sleeping Position of fetus
3
2
1
0





Symptoms Noon :




Drowsiness
6
4
2
0
Headache
3
2
1
0
Irritability
3
2
1
0
Hyperactive
3
2
1
0
Developmental Delay
3
2
1
0
School Performance
3
2
1
0





Hypertrophy ringWaldeye:








Mouth breathing
6
4
2
0
Chronic Rhinorhea
3
2
1
0
Reccurent tonsillitis
3
2
1
0





Physical examination:




Height
<5 percentile (6)
5-10 percentil (4)
>10 percentil (0)

BMI
<5/>95 percentile (6)
5-10/90-95 (4)
>10/<90 (0)

Blood pressure
>95 percentile (6)
>90/<95 (4)


Mouth breathing
4 (there)
0 (none)


Sound Hiponasal
4 (there)
0 (none)


Face adenoid
6 (heavy)
4 (mild)
0 (none)

Tonsil size
4 (6)
3 (4)
2 (2)
0 - 1 (0)
Severe sleep apnea recordings at moderate
severe apnea
moderate (6)
Tidak apnea (0)

severe adenoid
moderate
Mild hipertrofi
Normal (0)

hipertrofi (6)
hipertrofi (4)
-2

Echochardiography
Hipertensi pulmonal
Hipertensi



12
pulmonal








 Clinical Assessement highest total score is 164. Children - children with a score ≥ 40 has the possibility of OSA, a score ≥ 20 and ≤ 40 with moderate symptoms occur obtruksi upper airway but not panea, and children with a score ≤ 20 considered to be asymptomatic.
2.6.1 Polysomnography (PSG)Outcome apnea Polysomnography is, hipopnea, desaturasi index, total sleep time and sleep efficiency.Apnea sisefinisikan if the amplitude decreased by 80% or more in one or more businesses breath. Hipopnea defined as a decrease in 50-80% of the total amplitude pletysmography saturation associated with a reduction of 4% or more.Parameters measured during overhight Polysomnography includes elektoocolugam, electromeylogram (EMG), chest and abdominal wall motion, end-tidal CO2, transcutaneous oxygen (in children aged <8 years).PSG has tested positive for the occurrence of apnea and OSA apbila hipopnea per hour sleep (Respiration Disturbance Index, RDI) of at - least 5 or at least 10% of sleep time with oxygen saturation <90%. Within 6 months PSG evaluations performed to determine whether the patient would be surgery or not.When PSG is negative, patients are advised not to get a surgical therapy, although found symptoms - symptoms associated with enlarged tonsils and or adenoids.
2.6.2 Pulse OximetriOxygen saturation measured during PSG. At the time of the morning or after 12 hours pangukuran be obtained trend of oxygen saturation and heart rate. In the OSA children, apnea obtruksi desaturasi hipopnea and occur mainly in REM phase of sleep (Rapid Eye Movement). Desaturasi defined as a decrease in oxygen saturation of 4% or more.
2.7 Diagmosis appealDifferential diagnosis of OSA is the primary Snoring and upper airway resistance syndrome (UARS).
2.7.1 Primary SnoringChildren with primary Snoring show no clinical symptoms of day or night as well as children with OSA. Primary Snoring is expressed as a mild condition that will get better without special action on 50% of children. Marcus et al, 1998 on research to get less than 10% of children with primary Snoring in perjalanannnya will continue to be mild OSA.
2.7.2 Upper airway resistance syndrome (UARS)Terminology upper airway resistance syndrome (UARS) is widely used in adults to explain the current state of sleep breathing disorder characterized by apnea and hipopnea, but not dikatergorikan as OSA. UARS terminology can not be used in children - children. Gozall, 1998 refer to the term sleep-associated gas exchange abnoemalities (SAGEA) to explain the existence of hypoxemia and hypercarbia in the absence of apnea in children.The term "obtruksi hypoventilation" is also used to describe a partial obtruksi road, but the frequency and severity of apnea that occurred is not sufficient for diagnosing OSA.



2.8 ComplicationsComplications OSA is a combination of factors hypoxemia and hiperkapnea, business muscle - muscle that prolonged and neuropsi kologis and cognitive deficits due to poor sleep quality.OSA is not handled properly can cause failure to thrive (failure to thrive, FTT) and recurrence of upper airway infection. In children with developmental delay, episodes of hypoxia can be simultaneously with the aspiration that resulted in recurrence of respiratory infections.Chronic OSA can cause hypoplasia of the face. "Adenoid face" is a characteristic of obtruksi on pharing that can settle until adulthood.OSA in children showed disturbances in pemnusatan attention and intellectual abilities compared with healthy children's age. Gozall, 1998 get the capability of learning in children - children who snore without apnea during sleep compared with healthy child his age. Adenotonsilektomi action in some cases been reported to improve the intellectual abilities.
2.8.1 Management
2.8.2 Non-SurgicalIn some cases of OSA, non-surgical therapy is very limited. In rhinitis where the nasal airflow decrease, the use of topical nasal therapy anithistamin and to improve nasal airflow.Nasal steroids and oral leukotrine modifiers can be used to relieve symptoms of residual OSA after surgery performed.In children with micrognatis and dental malocclusion, handling orthodontis very helpful. Postural therapy is necessary for children with or retrognatia mikrognatia prone sleeping position is very helpful to position prevents the tongue that far back.CPAP (continuous positive airway pressure) therapy is widely used on nocturnal apnea in adult patients. Side effects are often found in the use of CPAP is vestibulitis and epistaxis.
  
2.8.3 Surgerya. Tensilektomi and AdenoidektomiCurrently tonsilketomi and adenoidektomi is an effective therapy of OSA in children. Polysomnography performed after surgery showed improvement in oxygen saturation and decreased episodes of apnea.b. Another surgery is rarely performed uvulopharyngopalatoplasty, epiglottoplasty and mandibular advancement procedure.c. Trakheotomi
2.9 PrognosisIn children with hypertrophic tonsils and adenoids that cause OSA adenoidektomi tonsillectomy and generally give satisfactory results even though no studies that reported it.In children with failure to thrive (failure to thrive), but OSA can improve somatic growth disorders. While the effect on cognitive impairment, has not found research that supports cognitive improvement in children with OSA.
2:10 Follow-upIn children with OSA and tonsillectomy surgical therapy adenoidektomi memeperbaiki good results in general and postoperative evaluation with polysomnography is not recommended. But in children with high-risk category, for example in children with a particular syndrome, the third son still got breath during sleep disturbance. In patients recommended to perform polysomnography test performed 6-8 weeks after surgery to confirm whether the patient requires additional therapy, including intranasal steroids and oral leukotrein modifier.Patients who received non-invasive ventilation requires repeated evaluation of polysomnography.
2:11 OSA in children with special needsChildren with certain syndromes and neurological disorders with developmental delay has a tendency to the occurrence of OSA. OSA occurs in about 50% of children with Down syndrome. Hipotonia pharing and makroglosis factor mentioned is the cause of OSA in patients with Down syndrome. In young cerebral palsy and Craniofacial syndrome, measures are often needed to trakheotomi in some specific cases.
3. SUMMARY AND CONCLUSIONSObstructive sleep apnea occurs frequently in children - children and require special attention to prevent complications. OSA can cause interference on growth and development and quality of life of children, recurrent aspiration and infections of the respiratory system.Adenotonsilektomi is definitive therapy in many cases and these actions can improve the quality of life in patients with OSA. OSA is more common and are more complex in children with kongential and other systemic disorders, whereas in the case - these cases are often required CPAP and trakheotomi.
REFERENCES1. Schecther MS. Technical report: Diagnosis and Management of Childhood obstructive sleep apnea syndrome. Pediatrics 2002; 109: 10-20.2. Goldstein NA, Pugazhendi V et al. Clinical assessement of pediatric obstructive sleep apnea. Pediatrics 2004; 114: 33-34.3. Marcus CL. Management of obstructive sleep apnea in Childhood. Curr Opin Pulm Med 1997; 3: 464-9.4. Hui S, Ying WK. Obstructive sleep apnea syndrome in children. HKMJ 1997; 3: 419-26.5. Murphy TD. Obtructive sleep apnea syndrome 2007. Retrieved fromhttp:www.emedicine.com / ped/topic2679.htm dated 10 September 2008.6. Broulitte RT, Fembach SA, Hunt CE. Obstructive sleep apnea in infans and children. J Pediatr 1982; 100: 31-40.7. Marcus CL. Pathophysiology of Childhood obstructive sleep apnea: current concepts. Respi. Physiol 2000; 119: 143-54.8. Rosen CL. Clinical features of obstructive sleep apnea syndrome in Otherwise Healty hipeventilation children. Pediatr. Pulmonol 1999; 27: 403-9.9. NA Goldstein, N Sculerati, Wasleben JA, Friedman DM, Rapoport DM. Clinical diagnosis of pediatric obstructive sleep apnea validated by polysomnography. Otolaryngol Head Neck Surg 1992; 118: 741 -4.10. Gaultier C. obstructive sleep apnea syndrome in Infants and children: established facts and unsettled issues. Thorax 1995; 50: 1024-10.11. Marcus CL, Carroll JL, Koerner CB, et al. Dterminant of Growth in children with obstructive sleep apnea syndrome. J Pediatr 1994; 125 (4): 556-62.12. American Academy of Pediatrics, Sections on Pediatrics Pulmonology, subcommite on pediatric sleep apnea syndrome. Clinical practice guidline: diagnosis menegement of Pediatrics obstructive sleep apnea syndrome. Pediatrcs 2002; 109: 74-12.13. Brouilette RT, Morielli A, Leimnais A, Waters KA, Luciano R, Dhucarme FM. Nocturnal pulse oxymetri as an Abbreviated testing modality for the Pediatrics obstructive sleep apnea. Pediatrics 2000; 105: 405-12.14. Gislason T, Benediktsdottir B. Snoring, nocturnal hypoxemia and episodes apnoiec Among children 6 months to 6 years old: an apidemiologic study of lower linit of prevalence. Chest 1995; 107: 936-66.15. Nixon GM, Kermack AS, Davis GM. Planning adenotonsilectomy in children with obstructive sleep apnea: the role of overnight oxymetry. Pediatrics 2004; 113: 19-25.16. Frank Y, Kravat RE, Pollack C, Weitzman ED. Obstructive sleep apnea and its therapy: clinical and polycsomnography manifestation. Pediatrics 1983; 71: 737-42


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