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Premium member Presentation Transcript Slide 1: OBSTRUCTIVE SLEEP APNEA SYNDROME IN CHILDREN นายแพทย์วิศรุต การุญบุญญานันท์ Fellow Chest QSNICH Mar 2011 for PediatricianCase presentation: Case presentation 6-year-old boy with loud snoring, restless sleep, enuresis, moderate adenotonsillar hypertrophy, severe ADHD symptoms, and poor academic performance The child has snored since infancy child ‘‘needs’’ a television in his bedroomSlide 3: hard to wake him up by 6:30 AM often irritable during the day Family history paternal enuresis that resolved at age 12 and ADHD. The mother is obese, snores, has daytime fatigue, and is suspected of having OSASPhysical exam: Physical exam body mass index is 15 kg/m 2 3+ tonsil size mouth breathing Others : normalNext steps ?: Next steps ? Overnight oxygen monitoring Polysomnography Adenotonsillectomy Intranasal steroid Leukotriene antagonist Other treatments?Slide 6: Definition Classification WHAT is it ?Slide 7: Snoring : Vibration of oropharyngeal soft tissue wall when attempt to breathe against increase UAW resistance during sleepClinical definition: Clinical definition Obstructive apnea >= 90% drop in signal amplitude of airflow for >=90% of entire event, at least 2 breaths there is effort to breath during apnea Central apnea absent of airflow >= 20 sec or at least 2 breaths Without respiratory effort Mixed ApneaClinical definition: Clinical definition Hypoventilation P ET CO 2 > 50 mmHg for 25% total sleep time P ET CO 2 peak > 53 mmHg Hypopnea >= 50% ↓ airflow >= 2 breaths , with 3 % oxygen desaturation , or with arousalClinical definition: Clinical definition Apnea index (AI) Number of obstructive and/or central apneic events per hour of sleep Obstructive Apnea index Number of obstructive apneic Hypopnea index Number of hypopnea Apnea- Hypopnea index (AHI) Summation of AI and Hypopnea indexOSAS: OSAS Primary snoring: I ncreased airway resistance without other symptoms Upper airway resistance syndrome: sleep disturbance with excessive daytime sleepiness, normal blood gas profile Obstructive hypopnea syndrome: hypopnea, sleep disturbance without desaturation OSA apnea, hypopnea, sleep disturbance with desaturationSlide 12: Pathophysiology Etiology WHY ?Pathophysiology: Pathophysiology 5 major predisposing factors Anatomic narrowing : Adenotonsillar hypertrophy (ATH), micrognathia, retrognathia Airway mechanics Neuromuscular compensation Inflammation / cytokine / leukotriene ObesityAnatomic narrowing: Anatomic narrowing Adenotonsillar hypertrophy Chronic rhinitis, swelling turbinate Micrognathia, Retrognathia Obesity Neuromuscular disorderAirway Mechanic: Airway Mechanic genioglossal activity is critical for maintenance of upper airway patency in healthy and micrognathic infantsNeuromuscular: Neuromuscular ปกติ ขณะหลับ ↓ muscle tone ของ upper airway +intercostal ร่างกายปรับเพิ่มการทำงานของ pharyngeal dilator activity OSA Sleep airway แคบลงเพราะ negative pressure ขณะหายใจเข้าPathogenesis of OSA: Pathogenesis of OSA White; AJRCCM 2005Down Syndrome: Down Syndrome OSAS = 54-100% Physical factors Small midface and cranium Narrow nasopharynx Large tongue Muscular hypotonia Obesity Small larynx Congenital heart disease / cor pulmonaleInflammation : Inflammation ตรวจพบ cysteinyl leukotriene (cys-LT) และ LT-receptor ในทอนซิลของเด็กที่ผ่าตัดออกเนื่องจาก OSA ตรวจพบ cys-LT ในลมหายใจออก และปัสสาวะของเด็ก OSA Pro-inflammatory : IL-6 ↑ Anti-inflammatory : IL-10 ↓ CRP, adhesion molecules เพิ่มสูงกว่าเด็กปกติObesity: Obesity Moderate OSA ↑ 12% / BMI ↑ 1 kg/m2 , but also depend on fat distribution OSA also relate with Mallampati score Adenotonsillectomy in obese child with OSA ↓ AHI, but 76% residual OSASObesity hypoventilation syndrome (Pickwickian syndrome): Obesity hypoventilation syndrome (Pickwickian syndrome) Obesity BMI>=30 kg/m 2 , Daytime hypercapnia, Sleep disordered breathing แยกจาก hypoventilation สาเหตุอื่น Neuromuscular dz, central hypoventilation Severe hypothyroidismSlide 23: Diagnosis HOW ?Pediatric OSAS: Pediatric OSAS 7-9% of children Males = Females Peak at age 3-6 Years old Physiologic lymphoid hyperplasia Frequent URI from school/ daycare Peak OSA = Peak ATHSlide 25: Symptoms Signs Investigation Diagnosis Nocturnal Symptoms: Nocturnal Symptoms Loud snoring Apneic pause Paradoxical movement Restless sleep Sweating during sleep Abnormal sleeping position Mouth breathing EnuresisDaytime Symptoms: Daytime Symptoms Poor school performance Short-term memory loss Impaired concentration Aggressive behavior ADHD Excessive daytime sleepiness Morning headaches (cerebral vasodilation)Physical exam: Physical exam General Obesity , Failure to thrive , Sleepiness Nose Swollen nasal mucous membranes Deviated septum Mouth Tonsillar hypertrophy , High-arched palate Elongated soft palate , Crowded oropharynx Macroglossia , Glossoptosis Face Midfacial hypoplasia , Allergic shiner, Adenoid facies, Micrognathia/retrognathia CVS Systemic hypertension , Loud P2 Extremities Edema , ClubbingMallampati Classification: Mallampati ClassificationSlide 33: Adenoid hypertrophy : รอยต่อ hard-soft palate ลากตั้งฉาก : > 67%Slide 34: Snoring Hx, PE, Film lateral neck Craniofacial anomalies Neuromuscular dz Cardiopulmonary dz Metabolic disorder No complicated underlying dz Persistent snoring Good response Significant desaturation Evaluating OSA F/U Primary snoring T&A or CPAP No significant desaturation OSA Polysomno graphy Overnight pulse oximetry Rx – Infection Allergy ObesityOvernight SpO2 monitor: Overnight SpO2 monitor Masimo, Nonin 1 จุด = 2 sec นับส่วนที่ SpO2 < 90% 10 จุด (20 sec) x 3 cluster Normal Sleep Architecture: Normal Sleep Architecture N1 sleep-wake transition N2 initiation of true sleep : K complex N3 deep sleep : delta wave Dreaming, autonomic, **SDB**Sleep Apnea Cycle: Sleep Apnea Cycle Ventilation Apnea Arousal Sleep Hypoxia Pleural pressure Δ Sympathetic activation ReoxygenationDIAGNOSIS: DIAGNOSIS OSAS severity : AHI mild 1–5 /h r moderate 5–10/h r severe >10 /h rDiagnostic classification of SDB: Diagnostic classification of SDB Dx AI (/hr) Nadir SpO2 P ET CO 2 peak P ET CO 2 >50 (%TST) Arousal (/hr) Primary snoring <=1 >92 <=53 <10 EEG<11 UARS <=1 >92 <=53 <10 EEG>11RERA>1 Mild OSA 1-4 86-91 >53 10-24 EEG>11 Mod OSA 5-10 76-85 >60 25-49 EEG>11 Severe OSA >10 <=75 >65 >=50 EEG>11 Marcus, Katz. Principles and practice of Pediatric Sleep Medicine. 2005Sequelae of Pediatric OSA: Sequelae of Pediatric OSA Metabolic sequelae Cardiovascular sequelae Neuropsychological sequelaeMetabolic sequelae: Metabolic sequelae Failure to thrive 27-62% ↓ IGF-1, IGFBP-3 Insulin resistance Dyslipidemia Hypertension Elevated C RPNeurocognitive: Neurocognitive Decreased quality of life Aggressive behavior Poor school performance Depression Attention deficit Hyperactivity MoodinessCardiovascular: Cardiovascular Autonomic dysfunction Systemic HT Absent BP ‘‘dipping’’ during sleep LV dysfunction P AH Abnormal HR variability Elevated vascular endothelial growth factorSlide 46: Treatment HOW ?Treatment: Treatment Depend on etiology, severity, natural history Allergic rhinitis : Intranasal steroid, antihistamine, Leukotriene antagonistTreatment: Treatment Intranasal steroid Leukotriene antagonists CPAP Uvulopharyngopalatoplasty (UPPP), genioglossus advancement, Maxillomandibular advancement TracheotomySlide 49: Snoring Hx, PE, Film lateral neck Craniofacial anomalies Neuromuscular dz Cardiopulmonary dz Metabolic disorder No complicated underlying dz Persistent snoring Good response Significant desaturation Evaluating OSA F/U Primary snoring T&A or CPAP No significant desaturation OSA Polysomno graphy Overnight pulse oximetry Rx – Infection Allergy ObesityIntranasal steroid: Intranasal steroid B eclomethasone ↓ adenoid/choanae ratio from 91% 77% at 1 month, and 62% after 6 months. intranasal duration AHI fluticasone 5 weeks 11 6 /h budesonide 6 weeks 3.7 1.3 /h budesonide 4 weeks 5.2 3.2 /hAdenotonsillectomy : T&A: Adenotonsillectomy : T&A 1 st line : Tonsillectomy & adenoidectomy Positive Airway Pressure (CPAP): Positive Airway Pressure (CPAP)Initiate CPAP when..: Initiate CPAP when.. AHI > 5 events/hr Profound gas exchange abnormalities : SpO2 < 90% Increase sleep fragmentation : Arousal index > 15 /hr Neurobehavior symptoms Severe OSAS polysomnographically Severe manifestations : FTT, PAH, marked aberration in daytime functioningCPAP: CPAP Properly fitted mask Proper CPAP level Side effects skin erythema eye irritation congestion, dryness, rhinorrhea maxillary growth impairmentadenotonsillectomy: adenotonsillectomy Following adenotonsillectomy, improve in quality of life Behavior , attention growth cognitive scores , school performanceRisk factors for postop. Respiratory complication after T&A: Risk factors for postop. Respiratory complication after T&A Age < 3 years obesity severe OSA S on polysomnography Failure to thrive Prematurity Recent respiratory infection N euro muscular disorders C raniofacial malformations residual OSAS more than 40% of cases postoperatively ( polysom .) AAP : Pediatrics 2002BiPAP for OHS / OSA: BiPAP for OHS / OSA เริ่มต้น IPAP/EPAP 8/2 cmH 2 O (IPAP – EPAP >= 6 หายใจสบาย และ adequate ventilation) เพิ่ม IPAP และ EPAP ทีละ 1 cmH 2 O เช่น 8/2 9/3 จนไม่มี obstructive apnea หลังจากนั้นให้คงค่า EPAP ไว้ที่เดิม เพิ่มแต่ IPAP จนมีลมเข้าถึงชายปอด 2 ข้าง ผู้ป่วยมักหายใจได้เอง ไม่ต้อง backup rate ถ้าผู้ป่วยมีการหยุดหายใจ เลือกเครื่องที่มี backup rateSurgical Treatment Options: Surgical Treatment Options Septoplasty Turbinoplasty Partial turbinectomy Polypectomy Excision of nasal tumours Adenoid tonsils excision Uvulopalatopharyngoplasty Tonsillectomy Uvulectomy Partial glossectomy/tongue base reduction Genioglossal advancement Lingual tonsils excision Hyoid advancement/suspension Maxillomandibular advancement Excision of laryngeal tumours TracheotomySlide 59: กลับมาที่ case demonstrationovernight polysomnography: overnight polysomnography respiratory disturbance index of 2 events per hour (most with arousal) 3% desaturation index of ten per hour, and no saturation values below 92% arousal index was 12 per hour. Most of the sleep time was in the prone or side position, with no REM supine sleep time recordedoptimal management: optimal management T&A reassessment of daytime functioning Rx ADHD if symptoms persist improv e sleep hygiene sleep time at least 10 hours television out of the bedroom behavioral management Mx enuresis ( behavioral , conditioning )ขอขอบพระคุณ อ.ประวิทย์ เจตนชัย: ขอขอบพระคุณ อ.ประวิทย์ เจตนชัย You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.
OSA Wiseroot Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 131 Category: Education License: Some Rights Reserved Like it (0) Dislike it (0) Added: August 13, 2011 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript Slide 1: OBSTRUCTIVE SLEEP APNEA SYNDROME IN CHILDREN นายแพทย์วิศรุต การุญบุญญานันท์ Fellow Chest QSNICH Mar 2011 for PediatricianCase presentation: Case presentation 6-year-old boy with loud snoring, restless sleep, enuresis, moderate adenotonsillar hypertrophy, severe ADHD symptoms, and poor academic performance The child has snored since infancy child ‘‘needs’’ a television in his bedroomSlide 3: hard to wake him up by 6:30 AM often irritable during the day Family history paternal enuresis that resolved at age 12 and ADHD. The mother is obese, snores, has daytime fatigue, and is suspected of having OSASPhysical exam: Physical exam body mass index is 15 kg/m 2 3+ tonsil size mouth breathing Others : normalNext steps ?: Next steps ? Overnight oxygen monitoring Polysomnography Adenotonsillectomy Intranasal steroid Leukotriene antagonist Other treatments?Slide 6: Definition Classification WHAT is it ?Slide 7: Snoring : Vibration of oropharyngeal soft tissue wall when attempt to breathe against increase UAW resistance during sleepClinical definition: Clinical definition Obstructive apnea >= 90% drop in signal amplitude of airflow for >=90% of entire event, at least 2 breaths there is effort to breath during apnea Central apnea absent of airflow >= 20 sec or at least 2 breaths Without respiratory effort Mixed ApneaClinical definition: Clinical definition Hypoventilation P ET CO 2 > 50 mmHg for 25% total sleep time P ET CO 2 peak > 53 mmHg Hypopnea >= 50% ↓ airflow >= 2 breaths , with 3 % oxygen desaturation , or with arousalClinical definition: Clinical definition Apnea index (AI) Number of obstructive and/or central apneic events per hour of sleep Obstructive Apnea index Number of obstructive apneic Hypopnea index Number of hypopnea Apnea- Hypopnea index (AHI) Summation of AI and Hypopnea indexOSAS: OSAS Primary snoring: I ncreased airway resistance without other symptoms Upper airway resistance syndrome: sleep disturbance with excessive daytime sleepiness, normal blood gas profile Obstructive hypopnea syndrome: hypopnea, sleep disturbance without desaturation OSA apnea, hypopnea, sleep disturbance with desaturationSlide 12: Pathophysiology Etiology WHY ?Pathophysiology: Pathophysiology 5 major predisposing factors Anatomic narrowing : Adenotonsillar hypertrophy (ATH), micrognathia, retrognathia Airway mechanics Neuromuscular compensation Inflammation / cytokine / leukotriene ObesityAnatomic narrowing: Anatomic narrowing Adenotonsillar hypertrophy Chronic rhinitis, swelling turbinate Micrognathia, Retrognathia Obesity Neuromuscular disorderAirway Mechanic: Airway Mechanic genioglossal activity is critical for maintenance of upper airway patency in healthy and micrognathic infantsNeuromuscular: Neuromuscular ปกติ ขณะหลับ ↓ muscle tone ของ upper airway +intercostal ร่างกายปรับเพิ่มการทำงานของ pharyngeal dilator activity OSA Sleep airway แคบลงเพราะ negative pressure ขณะหายใจเข้าPathogenesis of OSA: Pathogenesis of OSA White; AJRCCM 2005Down Syndrome: Down Syndrome OSAS = 54-100% Physical factors Small midface and cranium Narrow nasopharynx Large tongue Muscular hypotonia Obesity Small larynx Congenital heart disease / cor pulmonaleInflammation : Inflammation ตรวจพบ cysteinyl leukotriene (cys-LT) และ LT-receptor ในทอนซิลของเด็กที่ผ่าตัดออกเนื่องจาก OSA ตรวจพบ cys-LT ในลมหายใจออก และปัสสาวะของเด็ก OSA Pro-inflammatory : IL-6 ↑ Anti-inflammatory : IL-10 ↓ CRP, adhesion molecules เพิ่มสูงกว่าเด็กปกติObesity: Obesity Moderate OSA ↑ 12% / BMI ↑ 1 kg/m2 , but also depend on fat distribution OSA also relate with Mallampati score Adenotonsillectomy in obese child with OSA ↓ AHI, but 76% residual OSASObesity hypoventilation syndrome (Pickwickian syndrome): Obesity hypoventilation syndrome (Pickwickian syndrome) Obesity BMI>=30 kg/m 2 , Daytime hypercapnia, Sleep disordered breathing แยกจาก hypoventilation สาเหตุอื่น Neuromuscular dz, central hypoventilation Severe hypothyroidismSlide 23: Diagnosis HOW ?Pediatric OSAS: Pediatric OSAS 7-9% of children Males = Females Peak at age 3-6 Years old Physiologic lymphoid hyperplasia Frequent URI from school/ daycare Peak OSA = Peak ATHSlide 25: Symptoms Signs Investigation Diagnosis Nocturnal Symptoms: Nocturnal Symptoms Loud snoring Apneic pause Paradoxical movement Restless sleep Sweating during sleep Abnormal sleeping position Mouth breathing EnuresisDaytime Symptoms: Daytime Symptoms Poor school performance Short-term memory loss Impaired concentration Aggressive behavior ADHD Excessive daytime sleepiness Morning headaches (cerebral vasodilation)Physical exam: Physical exam General Obesity , Failure to thrive , Sleepiness Nose Swollen nasal mucous membranes Deviated septum Mouth Tonsillar hypertrophy , High-arched palate Elongated soft palate , Crowded oropharynx Macroglossia , Glossoptosis Face Midfacial hypoplasia , Allergic shiner, Adenoid facies, Micrognathia/retrognathia CVS Systemic hypertension , Loud P2 Extremities Edema , ClubbingMallampati Classification: Mallampati ClassificationSlide 33: Adenoid hypertrophy : รอยต่อ hard-soft palate ลากตั้งฉาก : > 67%Slide 34: Snoring Hx, PE, Film lateral neck Craniofacial anomalies Neuromuscular dz Cardiopulmonary dz Metabolic disorder No complicated underlying dz Persistent snoring Good response Significant desaturation Evaluating OSA F/U Primary snoring T&A or CPAP No significant desaturation OSA Polysomno graphy Overnight pulse oximetry Rx – Infection Allergy ObesityOvernight SpO2 monitor: Overnight SpO2 monitor Masimo, Nonin 1 จุด = 2 sec นับส่วนที่ SpO2 < 90% 10 จุด (20 sec) x 3 cluster Normal Sleep Architecture: Normal Sleep Architecture N1 sleep-wake transition N2 initiation of true sleep : K complex N3 deep sleep : delta wave Dreaming, autonomic, **SDB**Sleep Apnea Cycle: Sleep Apnea Cycle Ventilation Apnea Arousal Sleep Hypoxia Pleural pressure Δ Sympathetic activation ReoxygenationDIAGNOSIS: DIAGNOSIS OSAS severity : AHI mild 1–5 /h r moderate 5–10/h r severe >10 /h rDiagnostic classification of SDB: Diagnostic classification of SDB Dx AI (/hr) Nadir SpO2 P ET CO 2 peak P ET CO 2 >50 (%TST) Arousal (/hr) Primary snoring <=1 >92 <=53 <10 EEG<11 UARS <=1 >92 <=53 <10 EEG>11RERA>1 Mild OSA 1-4 86-91 >53 10-24 EEG>11 Mod OSA 5-10 76-85 >60 25-49 EEG>11 Severe OSA >10 <=75 >65 >=50 EEG>11 Marcus, Katz. Principles and practice of Pediatric Sleep Medicine. 2005Sequelae of Pediatric OSA: Sequelae of Pediatric OSA Metabolic sequelae Cardiovascular sequelae Neuropsychological sequelaeMetabolic sequelae: Metabolic sequelae Failure to thrive 27-62% ↓ IGF-1, IGFBP-3 Insulin resistance Dyslipidemia Hypertension Elevated C RPNeurocognitive: Neurocognitive Decreased quality of life Aggressive behavior Poor school performance Depression Attention deficit Hyperactivity MoodinessCardiovascular: Cardiovascular Autonomic dysfunction Systemic HT Absent BP ‘‘dipping’’ during sleep LV dysfunction P AH Abnormal HR variability Elevated vascular endothelial growth factorSlide 46: Treatment HOW ?Treatment: Treatment Depend on etiology, severity, natural history Allergic rhinitis : Intranasal steroid, antihistamine, Leukotriene antagonistTreatment: Treatment Intranasal steroid Leukotriene antagonists CPAP Uvulopharyngopalatoplasty (UPPP), genioglossus advancement, Maxillomandibular advancement TracheotomySlide 49: Snoring Hx, PE, Film lateral neck Craniofacial anomalies Neuromuscular dz Cardiopulmonary dz Metabolic disorder No complicated underlying dz Persistent snoring Good response Significant desaturation Evaluating OSA F/U Primary snoring T&A or CPAP No significant desaturation OSA Polysomno graphy Overnight pulse oximetry Rx – Infection Allergy ObesityIntranasal steroid: Intranasal steroid B eclomethasone ↓ adenoid/choanae ratio from 91% 77% at 1 month, and 62% after 6 months. intranasal duration AHI fluticasone 5 weeks 11 6 /h budesonide 6 weeks 3.7 1.3 /h budesonide 4 weeks 5.2 3.2 /hAdenotonsillectomy : T&A: Adenotonsillectomy : T&A 1 st line : Tonsillectomy & adenoidectomy Positive Airway Pressure (CPAP): Positive Airway Pressure (CPAP)Initiate CPAP when..: Initiate CPAP when.. AHI > 5 events/hr Profound gas exchange abnormalities : SpO2 < 90% Increase sleep fragmentation : Arousal index > 15 /hr Neurobehavior symptoms Severe OSAS polysomnographically Severe manifestations : FTT, PAH, marked aberration in daytime functioningCPAP: CPAP Properly fitted mask Proper CPAP level Side effects skin erythema eye irritation congestion, dryness, rhinorrhea maxillary growth impairmentadenotonsillectomy: adenotonsillectomy Following adenotonsillectomy, improve in quality of life Behavior , attention growth cognitive scores , school performanceRisk factors for postop. Respiratory complication after T&A: Risk factors for postop. Respiratory complication after T&A Age < 3 years obesity severe OSA S on polysomnography Failure to thrive Prematurity Recent respiratory infection N euro muscular disorders C raniofacial malformations residual OSAS more than 40% of cases postoperatively ( polysom .) AAP : Pediatrics 2002BiPAP for OHS / OSA: BiPAP for OHS / OSA เริ่มต้น IPAP/EPAP 8/2 cmH 2 O (IPAP – EPAP >= 6 หายใจสบาย และ adequate ventilation) เพิ่ม IPAP และ EPAP ทีละ 1 cmH 2 O เช่น 8/2 9/3 จนไม่มี obstructive apnea หลังจากนั้นให้คงค่า EPAP ไว้ที่เดิม เพิ่มแต่ IPAP จนมีลมเข้าถึงชายปอด 2 ข้าง ผู้ป่วยมักหายใจได้เอง ไม่ต้อง backup rate ถ้าผู้ป่วยมีการหยุดหายใจ เลือกเครื่องที่มี backup rateSurgical Treatment Options: Surgical Treatment Options Septoplasty Turbinoplasty Partial turbinectomy Polypectomy Excision of nasal tumours Adenoid tonsils excision Uvulopalatopharyngoplasty Tonsillectomy Uvulectomy Partial glossectomy/tongue base reduction Genioglossal advancement Lingual tonsils excision Hyoid advancement/suspension Maxillomandibular advancement Excision of laryngeal tumours TracheotomySlide 59: กลับมาที่ case demonstrationovernight polysomnography: overnight polysomnography respiratory disturbance index of 2 events per hour (most with arousal) 3% desaturation index of ten per hour, and no saturation values below 92% arousal index was 12 per hour. Most of the sleep time was in the prone or side position, with no REM supine sleep time recordedoptimal management: optimal management T&A reassessment of daytime functioning Rx ADHD if symptoms persist improv e sleep hygiene sleep time at least 10 hours television out of the bedroom behavioral management Mx enuresis ( behavioral , conditioning )ขอขอบพระคุณ อ.ประวิทย์ เจตนชัย: ขอขอบพระคุณ อ.ประวิทย์ เจตนชัย