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Leyla Akanli, M.D. F.A.A.P F.C.C.P Pediatric Pulmonology and Sleep Medicine PEDIATRIC OBSTRUCTIVE SLEEP APNEA.

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Presentation on theme: "Leyla Akanli, M.D. F.A.A.P F.C.C.P Pediatric Pulmonology and Sleep Medicine PEDIATRIC OBSTRUCTIVE SLEEP APNEA."— Presentation transcript:

1 Leyla Akanli, M.D. F.A.A.P F.C.C.P Pediatric Pulmonology and Sleep Medicine PEDIATRIC OBSTRUCTIVE SLEEP APNEA

2 DEFINITIONS Sleep-disordered breathing (SDB) refers to the clinical spectrum of repetitive episodes of complete or partial obstruction of the airway during sleep.  Primary Snoring (PS) Snoring without obstructive apnea, frequent arousals from sleep, or gas exchange abnormalities.  Obstructive Hypoventilation Syndrome (OHS) Persistent partial upper airway obstruction associated with gas exchange abnormalities, rather than discrete, cyclic apneas.  Upper Airway Resistance Syndrome (UARS) Increasingly negative intrathoracic pressures during inspiration that lead to arousals and sleep fragmentation.  Obstructive sleep apnea (OSA) Disorder of breathing during sleep characterized by prolonged partial upper airway obstruction and/or intermittent complete obstruction.

3 PRIMARY SNORING  Snoring is related to upper airway narrowing  Can not be diagnosed on clinical basis alone  PSG shows  No sleep fragmentation  No discrete events  No desaturation  No hypercapnia  PSG is essential to differentiate from PS from OSA  Clinical consequences of PSD is unknown

4 UPPER AIRWAY RESISTANCE SYNDROME-UARS  Snoring is due to upper airway narrowing or floppiness  Clinical history suggestive sleep fragmentation  PSG shows  Increased intra-thoracic pressure swings  Flow limitation of nasal pressure monitoring  Non –REM asynchronous breathing  Increased arousals  No gas exchange abnormalities  PSG is essential to differentiate UARS from OSA

5 OBSTRUCTIVE HYPOVENTILATION  Prolonged periods of partial airway obstruction  More common in children than adults  Clinical history similar to OSA  PSG demonstrates  Asynchronous breathing  Absence of discrete events  Sleep fragmentation  Abnormal gas exchange – maybe present only during REM sleep –Hypoxia, Hypercarbia PetCO2 > 53 torr

6 MILESTONES  1837 – Dickens – describes overweight/hypersomnolent boy in the Posthumous papers of the Pickwick Club (term “pickwickian” used by Osler)  1907- Osler  1973-Guilleminault  W. Hill described the obstructive sleep apnea sufferer child as in 1889; “ The stupid -lazy child who frequently suffers from headaches at school, breathes through his mouth instead of his nose, snores and restless at night and wakes up with a dry mouth in the morning is well worthy of the solicitous attention of the Scholl medical officer.”

7 ADULT VS PEDIATRIC OSA Pediatric OSA Adult OSA AgePreschoolElderly GenderM=FM>F EtiologyAdenoid/ Tonsil hypertrophy Obesity WeightFTT, normal, or obese Obese BehavioralHyperactiveSomnolent Sleep architecture NormalDecreased delta and REM sleep Surgical RxT&AUPPP Medical RxCPAP (rarely)CPAP

8 EPIDEMIOLOGY  Most studies showed 4% to 11% prevalence of parent- reported apnea.  Depending on threshold of AHI to diagnose, the prevalence of pediatric OSA ranges from 1% to 4% in most studies.  Children with abnormal PSG that go untreated will continue to have abnormal findings.  Snoring and adverse neurocognitive, neurobehavioral outcomes  Overall prevalence of snoring in pediatric patient population 8% and 5% in infants  Always snoring in 1.5%-6%

9 EPIDEMIOLOGY  Peaks ages two to 8 years  As obesity is increasing in pediatrics the age distributed shifted  Gender distribution: M>F after puberty, equal pre-puberty  Prevalence is higher among African Americans and Asian children  Family history  Prematurity  Other Co-Morbid conditions

10 PATHOPHYSIOLOGY Neuromotor tone Cerebral palsy Genetic diseases Structural factors Adenotonsillar hypertrophy Craniofacial abnormality Obesity Other factors Genetic Hormonal ? Diet, Inflammation, Passive smoking OSA Anatomic narrowing Requires increased inspiratory pressures Abnormal neuromuscular control Reflex activation of dilators in response to airway obstruction often fails

11 RISK FACTORS Adenotonsillar Hypertrophy Upper airway congestion; allergies Upper airway obstruction, choanal stenosis, larnygomalacia, subglottic stenosis GER/LPR Cleft palate Craniofacial dsymorphism : Mid -facial hypoplasia –Down’s syndrome Micrognothia – Pierre-Robin syndrome Cranial base malformation- Achondroplasia Neuromuscular disorder: Hypotonia-Down’s syndrome, Muscular dystrophy Spasticity –Cerebral Palsy Overweight Sickle cell disease Cystic fibrosis Chronic lung disease/ BPD Scoliosis Brain and spinal disorders – Spin Bifida, ACM type II

12  Trisomy 21 Small midface and cranium Relatively narrow nasopharynx Macroglossia Hypotonia Tendency for obesity Relatively small larynx  In addition, given their congenital heart defects, they are already predisposed to cor pulmonale.  Because of these factors, the incidence of OSA in patients with DS has been estimated to be from 54% to 100%. REDUCED MUSCLE TONE

13  Neuromuscular disease  Hypothyroidism  Cerebral Palsy  Moebius, MG  Reduced Central Ventilatory Drive ACM type I/II Myelomeningocele Brainstem injury or masses

14 MEDICAL CONDITIONS Craniofacial syndromes Apert Crouzon Pierre-robin Treacher-Collins Pfeiffer Miscellaneous Achondroplasia Beckwith-Wiedeman Goldenhar Marfan Mucopolysaccoridoses Prader Willi Sickle Cell Disease Prematurity /CLD

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16 CLINICAL FEATURES Nocturnal Symptoms Symptoms vary by age-especially in infants! Snoring-Volume does not correlate with the degree of obstruction Observed apneic pauses Snorting / gasping / choking Restless sleep Diaphoresis Paradoxical chest wall movement Abnormal sleeping position Sweating Mouth Breathing Secondary enuresis

17 CLINICAL FEATURES Daytime Symptoms-Physical and Behavioral Morning headaches Difficulty awakening in AM Hyponasal Speech Nasal congestion, Chronic Rhinorhea Mouth breathing, Dry Mouth Frequent infections Difficulty swallowing Poor appetite Daytime somnolence-7-10% Mood changes Internalizing behaviors Externalizing behaviors ADHD Like symptoms, School problems

18 ASSOCIATED FEATURES  Increase in partial arousal parasomnias  Worsening GERD  Increase in seizure frequency in predisposed children  Other CO-Morbid Sleep problems RLS,PLMS Circadian Rhythm Disorders Bedtime resistance, nightwakings

19 EVALUATION  Medical History Developmental and School history Family History Behavioral assessment  Physical Examination Growth HEENT Cardiac examination  Diagnostic Tests For the most part are unnecessary  Radiologic Studies Lateral Neck Laryngoscopy EKG/ECHO Cine-MRI

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21 MALLAMPATI CLASSIFICATION

22 MULLER MANEVEUR

23 LARNYGOMALACIA

24 SUBGLOTTIC STENOSIS

25 GERD

26 MRI Excellent soft tissue anatomy Multiple planes No ionizing radiation Disadvantages Cost Weight limitations Noisy claustrophobia

27 HOME OXIMETRY TESTING  Readily available and relatively inexpensive  Subject to presence of significant artifact  Artifact reduction maybe accomplished with simultaneous –heart rate measurement and Pletsymography waveform  Excellent positive predictive value-97%*  Poor negative predictive value-47%*  Disorders with predominant sleep disruption and hypercapnia will be missed. *Brouillette RT et al. Pediatrics 2000

28 NAP STUDY  Child may not achieve natural sleep – REM sleep may not be captured  Severity may be underestimated- Events usually worsens as the sleep progress  Excellent positive predictive value-77-100%*  Poor negative predictive value-17-49%* Keens TG, et al.Pediatric Pulmonol 1992, &Chest 2000

29 POLYSOMNOGRAPHY  PSG IS THE GOLD STANDARD  Meet diagnostic criteria of pediatric OSAS according to ICSD 2  Differentiate OSA from other SDB  Define severity of OSAS  Screen high risk children  Evaluate success of treatment  Titrate PAP therapy

30 POLYSOMNOGRAPHY  It should be performed without sedation and sleep deprivation  In a child- friendly environment  By personnel with training in recording and scoring pediatric PSG’s  Should be interpreted by physicians with expertise in pediatric sleep medicine

31 Courtesy of Dr. Carol Rosen PEDIATRIC POLYSOMNOGRPAHY Tech Observer Video Camera Sao2 Leg EMG (2) Microphone EKG Chin EMG (2) EEG EOG Nasal EtCO2 Record behavior Documents arousals, parasomnias, abnormal sleeping position, and attends to any technical problem Respiratory Effort Nasal Oral Airflow

32 PSG PARAMETERS  Apnea Any pause in respiration lasting longer than two breaths.  Versus at least 10 s in adults.  Hypopnea Reduction of airflow by 50% for two respiratory cycles accompanied by reduction of saturation by 3% or arousal from sleep.  AHI Sum of Apneas and Hypopneas per hour of sleep.  RDI Sum of Apneas, Hypopneas, and respiratory event-related arousals per hour of sleep.  No universally accepted PSG normal reference values  AHI >1.5 or AI >1 per hour is most often used to identify children- up to 12 years with OSA.  Oxygen saturation<91%  Change in nadir 02 from baseline>9%  Maximal ETCO2>54

33 PEDIATRIC POLYSOMNOGRAPHY In contrast to adults, children have: Obstructive hypoventilation Fewer obstructive apneas Desaturation with shorter events –Higher respiratory rate –Lower functional residual capacity –Smaller oxygen store

34 PEDIATRIC OSA -SEVERITY OSA SEVERITY LEVEL AHISpO2 NADIR % PEAK ETCO2 TORR PEAK ETCO2 > 5O T0rr %TST MILD1-486-91>5310-24 MODERATE5-1076-85>6025-49 SEVERE>10<75>65>50

35 PARADOXICAL RIB-CAGE MOTION HYPERCAPNIA

36 OBSTRUCTIVE APNEA This tracing depicts cyclic obstructive apneas

37 MANAGEMENT Any child with AHI> 5 intervention is necessary. Less of a consensus regarding AHI 1-5.  Surgical –Adenotonsillectomy – First Line of therapy –Turbinate reduction –Craniofacial surgery- Mandibular advancement Lefort osteotomies and maxillary distraction. –Uvulopalatopharyngoplasty- Not a good idea ! –Tracheostomy  Medical –Weight loss –Continuous positive airway pressure –Intranasal steroids (modest effect)-Mild patients –Leukotriene antagonist- Mild patients –Oral appliances –Positional therapy –Snore aids

38 ADENOTONSILLECTOMY  First-line of treatment  Presence of additional risk factors not a contraindication to adenotonsillectomy  25 % residual OSA  Re-assessment of high risk groups with post-operative polysomnography is recommended  CHAT study –RCT 5-9 years old

39 HIGH RISK PATIENTS Risk Factors for Postoperative Respiratory Complications in Children with OSAS undergoing Adenotonsillectomy –Age Younger than 3 years –Severe OSAS on PSG, AHI>10 –Pulmonary hypertension –Congenital heart disease –FTT –Prematurity, CLD. –Recent URI – Morbid Obesity –Trisomy 21 –Craniofacial abnormalities –Neuromuscular disorders, CP –Asthma

40 SEVERE OSA  Children with severe OSA show a significant improvement in RDI and quality of life.  OSA does not resolve in the majority of these patients.  Postoperative PSG is recommended for all children with severe OSA.  To identify those who may require further therapy.

41 SEVERE OSA

42 CPAP  Almost always an alternative to surgery  Surgical failure;  Morbid Obesity  Complex OSA  Non-Surgical candidates  Local and systemic anti-inflammatory effect  Act as a pneumatic splint  Stimulates ventilation  Reduces activity of inspiratory, upper airway muscles and diaphragm  Restores sleep, promotes weight loss  Improves cardiac function, Suppresses GERD  Decrease AHR  FDA approved for children > 30 kg

43 CPAP

44 CPAP-AIRWAY

45 Management Algorithm

46 COMPLICATIONS OF OSA  Effects on growth  Neurocognitive morbidity  Cardiovascular consequences  Metabolic

47 IMPROVEMENT IN WEIGHT Marcus et al. J Pediatr 1994 Girls Boys

48 NEUROCOGNITIVE MORBIDITY  Hyperactivity, inattention, aggression  Impaired school performance  Daytime sleepiness  Depression

49 CARDIOOVASCULAR MORBIDITY  Pulmonary Hypertension  Cor Pulmonale  Systemic Hypertension

50 HYPERTENSION

51 Marcus et al. Am J Respir Crit Care Med 1998

52 AAP GUIDELINES  Screening of all children for snoring  Specialty referral of complex high-risk patients  Urgent evaluation of cardio-respiratory failure  PSG as Gold Standard for diagnosis  Adenotonsillectomy as first-line treatment  Inpatient monitoring of high-risk patients  Post-operative reevaluation to determine if additional treatment is required


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