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

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 Age Preschool Elderly
Gender
M=F
M>F
Etiology
Adenoid/
Tonsil
hypertrophy
Obesity
Weight
FTT, normal, or obese
Obese
Behavioral
Hyperactive
Somnolent
Sleep architecture
Normal
Decreased delta and REM sleep
Surgical Rx
T&A
UPPP
Medical Rx
CPAP (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
Pediatric OSA is a common disorder which is most likely under-diagnosed. Up to 20% of normal children snore intermittently and 7% to 10% of children are habitual or regular snorers.22, 23 Current best estimates suggest that 1% to 3% of preschool children have significant disease.24 The age distribution of OSA corresponds to the peak period of lymphoid hyperplasia and adenotonsillar hypertrophy in children, which may be a contributing factor for pediatric OSA. Unlike adults, gender distribution in children, at least during the prepubertal years, is approximately equal.
22. Ali NJ, Pitson D, Stradling JR. Natural history of snoring and related behaviour problems between the ages of 4 and 7 years. Arch Dis Child 1994;71(1):74-6.
23. Gislason T, Benediktsdottir B. Snoring, apneic episodes, and nocturnal hypoxemia among children 6 months to 6 years old. An epidemiologic study of lower limit of prevalence. Chest 1995;107(4):963-6.
24. Redline S, Tishler PV, Schluchter M, Aylor J, Clark K, Graham G. Risk factors for sleep-disordered breathing in children. Associations with obesity, race, and respiratory problems. Am J Respir Crit Care Med 1999;159(5 Pt 1):

10. PATHOPHYSIOLOGY OSA Neuromotor tone Structural factors Other factors
Cerebral palsy
Genetic diseases
Structural factors
Adenotonsillar hypertrophy
Craniofacial abnormality
Obesity
OSA
Other factors
Genetic
Hormonal
? Diet, Inflammation, Passive smoking
The etiology of pediatric OSA is not yet fully understood. It is thought to be due to a combination of structural, neuromotor and other factors. Structural factors result in upper airway narrowing; this may be due to adenotonsillar hypertrophy or craniofacial anomalies (e.g., micrognathia, midfacial hypoplasia). Obesity increases the risk for OSA by some combination of increasing the pharyngeal resistive load, increasing the compliance of the pharynx, or other mechanisms. Abnormal neuromotor tone is a prominent factor in some children with OSA, such as those with cerebral palsy. However, subtle abnormalities in upper airway neuromotor control are probably present in all patients with OSA - if not, these patients would obstruct during wakefulness as well as sleep. Subclinical neuromotor abnormalities may explain why some children with adenotonsillar hypertrophy develop OSA, whereas other children with similarly enlarged tonsils and adenoids do not. Other factors include a genetic predisposition, hormonal effects (particularly testosterone), and probably other, as yet undefined, factors.
A combination of structural, neuromotor and other factors are necessary for the development of OSA. However, the degree to which each factor contributes will differ. Thus, in a child with severe craniofacial anomalies, upper airway narrowing may predominate, whereas in a child with muscular dystrophy, decreased upper airway tone may predominate.
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. REDUCED MUSCLE TONE 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%.
A retrospective review of patients with a diagnosis of Down syndrome who underwent tonsillectomy and/or adenoidectomy. The study was conducted to identify early postoperative morbidity and to evaluate results of the surgery. Only one of the 16 patients had sleep studies pre-operatively

13. REDUCED MUSCLE TONE 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

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
Symptoms suggestive of OSAS include those related to nighttime events, and those that represent daytime consequences. As in adults, loud, disruptive, continuous and habitual snoring is the most common symptom of OSAS in children.
Parents may describe apneas or breathing pauses, often followed by snorting or gasping. Parents may describe their child struggling to breathe with paradoxical chest wall movement, i.e., out of phase rib cage and abdominal movements. Parents may express considerable anxiety about these apnea episodes, and may report shaking the child during sleep to stimulate breathing or even bringing the child into the parental bed.28
Children with OSAS are often described as having very restless and fitful sleep, moving around frequently, “tossing and turning,” and sweating during sleep. They may sleep with their necks hyperextended, sitting upright with several pillows or other unusual positions in an attempt to reduce the obstruction. Secondary enuresis, or the recurrence of bedwetting in a child previously dry at night, may also occur in association with OSAS.29
28. Brouillette RT, Fernbach SK, Hunt CE. Obstructive sleep apnea in infants and children. J Pediatr 1982;100(1):31-40.
29. Weider DJ, Sateia MJ, West RP. Nocturnal enuresis in children with upper airway obstruction. Otolaryngol Head Neck Surg 1991;105(3):

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
Young children with sleep fragmentation are more likely to manifest daytime sleepiness behaviorally, through increased activity, aggression, poor concentration, and irritability rather than to act or complain of feeling “sleepy.” Children with OSAS may have difficulty awakening in the morning despite having what appears to be adequate time in bed. Morning headaches may be a result of hypercapnia or hypoxia. Children with upper airway obstruction may have mouth breathing, halitosis, nasal congestion, and Rhinorhea, as well as Hyponasal voice.

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 Physical Examination Diagnostic Tests
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

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 %*
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
The ICSD 221 diagnostic criteria for pediatric OSA incorporates polysomnographic criteria as well, making pediatric polysomnography essential for diagnosing pediatric OSA. Additionally, polysomnography is performed to confirm the diagnosis of obstructive sleep apnea when it is suspected on clinical grounds, and to differentiate between OSA and primary snoring. Polysomnography helps to delineate the severity of the OSA, since this will affect the choice of treatment and degree of postoperative monitoring. Polysomnography should be considered to evaluate symptoms such as excessive daytime sleepiness or failure to thrive. Finally, a polysomnogram may be necessary to evaluate the success of an intervention, such as adenotonsillectomy, particularly in a situation in which post-treatment residual symptoms or risk factors for OSA exist, or when OSA was severe prior to treatment.
21. American Academy of Sleep Medicine. International classification of sleep disorders. 2 ed. Westchester, IL: American Academy of Sleep Medicine; 2005.

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. PEDIATRIC POLYSOMNOGRPAHY
EEG
EOG
Nasal EtCO2
Nasal Oral Airflow
Chin EMG (2)
Microphone
Sao2
EKG
Tech Observer
Video Camera
This illustration shows the standard types of monitoring devices used in pediatric polysomnographic evaluation in most sleep laboratories. Electroencephalography (EEG), electro-oculography (EOG) and submental electromyography (EMG) are used to monitor sleep architecture and arousals. The presence of airflow is assessed by nasal/oral thermistors and/or capnography and/or pressure transducers. Chest wall excursion is usually measured by means of inductance plethysmography or strain gauges. Intercostal EMG can be used to measure respiratory effort, particularly paradoxical chest wall movement. A pulse oximeter measures oxygenation. CO2 is generally assessed either by means of a transcutaneous CO2 monitor or an end-tidal CO2 probe; this is helpful to assess hypoventilation. The entire procedure is observed by a technician who documents arousals, parasomnias, abnormal sleeping position, and attends to any technical problem. Esophageal pH may be monitored if gastroesophageal reflux is a clinical consideration.
Children usually require advance preparation, which may include a tour of the sleep lab prior to the polysomnographic evaluation. It generally requires more time and patience to set up a child for a polysomnogram, and it is usually helpful if a parent is present during the study. The sleeping room should be child-friendly, and technicians in the sleep lab should be comfortable and familiar working with children.30
30. Zaremba EK, Barkey ME, Mesa C, Sanniti K, Rosen CL. Making polysomnography more "child friendly:" A family-centered care approach. Journal of Clinical Sleep Medicine 2005;1(2):
Respiratory Effort
Documents arousals, parasomnias, abnormal sleeping position, and attends to any technical problem
Leg EMG (2)
Record behavior
Courtesy of Dr. Carol Rosen

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
The polysomnographic findings of pediatric OSA often differ from those typically found in adults on a number of important parameters.
Obstructive hypoventilation with periods of hypercapnia, desaturation, or hypercapnia and desaturation associated with snoring, paradoxical inward rib-cage motion during inspiration, and with either, markedly negative esophageal pressure swings or frequent arousals from sleep may be present. In general, children have fewer clear obstructive events than do adults. An apnea-hypopnea index (or the number of respiratory events per hour of sleep), of 5 or greater is considered abnormal in young adults, whereas normal children usually do not have more than one obstructive apnea per hour of sleep. However, the clinical significance of a small number of respiratory events, even if statistically abnormal, is not known. Children are also more likely to have significant O2 desaturation with shorter obstructive events than do adults, probably due to a lower functional residual capacity and smaller oxygen stores.31, 32
31. Marcus CL, Omlin KJ, Basinki DJ, et al. Normal polysomnographic values for children and adolescents. Am Rev Respir Dis 1992;146(5 Pt 1):
32. Uliel S, Tauman R, Greenfeld M, Sivan Y. Normal Polysomnographic Respiratory Values in Children and Adolescents. Chest 2004;125(3):872-8.

34. PEDIATRIC OSA -SEVERITY
LEVEL
AHI
SpO2 NADIR %
PEAK ETCO2
TORR
PEAK ETCO2 > 5O T0rr
%TST
MILD
1-4
86-91
>53
10-24
MODERATE
5-10
76-85
>60
25-49
SEVERE
>10
<75
>65
>50
ADOPTED FROM MARCUS ET AL-DIAGNOSIS OF OSA IN CHILDREN IN PRNCIPLES AND PRACTICE OF SLEEP MEDICINE.

35. PARADOXICAL RIB-CAGE MOTION
This tracing depicts obstructive hypoventilation, i.e. persistent partial upper airway obstruction associated with hypercapnia. The child, who was snoring at the time, has paradoxical inward rib cage motion. There are no obstructions - airflow can be seen for each respiratory effort. The partial obstruction has resulted in severe hypoxemia (SaO2 in the 60s) and hypercapnia (end-tidal pCO2 in the 70s). This pattern can occur for prolonged periods of time without arousal from sleep.
HYPERCAPNIA

36. This tracing depicts cyclic obstructive apneas
Two patterns of obstruction occur in children with OSAS. This tracing depicts cyclic obstructive apneas, similar to that seen in adults. There are several episodes of obstructive apnea (evidenced by lack of airflow on both the oronasal (NAF) and pCO2 channels) despite continued respiratory effort. This is associated with oxyhemoglobin desaturation to 81%.
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
Adenotonsillectomy has been demonstrated in a number of studies to be an effective first-line treatment for pediatric OSA Since OSA results from relative narrowing of upper airway rather than the absolute size of the tonsils and adenoids, tonsillar size should not be a deciding factor on whether to operate or not. Adenotonsillectomy has been shown to be an effective treatment even in those patients who have additional risk factors, such as Down syndrome. For children with severe apnea, adenotonsillectomy alone may not result in complete resolution of OSA and a repeat polysomnogram should be considered 4 to 8 weeks post-operatively.
50. Frank Y, Kravath RE, Pollak CP, Weitzman ED. Obstructive sleep apnea and its therapy: clinical and polysomnographic manifestations. Pediatrics 1983;71(5):
51. Potsic WP, Pasquariello PS, Baranak CC, Marsh RR, Miller LM. Relief of upper airway obstruction by adenotonsillectomy. Otolaryngol Head Neck Surg 1986;94(4):
52. Suen JS, Arnold JE, Brooks LJ. Adenotonsillectomy for treatment of obstructive sleep apnea in children. Arch Otolaryngol Head Neck Surg 1995;121(5):

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
Study on 29 children 1-18 years of age with RDIs > 30 that underwent adenotonsillectomy followed by PSG 6 months postoperatively. Subjects were classified as “cured” if their RDI < 5, mild OSA if 5-10, moderate if 10-30, and severe if > 30. Did not stratify results between pre-op and post-op scores.

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
Study of 20 consecutive patients with refractory OSA that underwent aggressive skeletal and soft-tissue surgery to avoid tracheostomy. The patients had underlying conditions such as cri du chat, down syndrome, pierre-robin syndrome, CP, etc. As a result of the algorithm proposed by this group, most of the patients were spared the morbidity of tracheostomy.

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

47. IMPROVEMENT IN WEIGHT Girls Boys
Failure to thrive (FTT) as a consequence of pediatric OSA has been documented in earlier reports Presentation of OSA in this manner has become less common, probably due to earlier recognition and treatment of the condition. In a small study of children with OSA and FTT catch-up growth was noted after adenotonsillectomy in all children. Adenotonsillectomy has also been shown to increase the height and weight velocities of children with normal growth and OSA. This is also true of obese children who undergo adenotonsillectomy for OSA. The mechanisms of failure to thrive in children with OSA are not completely understood but are likely related to an increase in night-time energy expenditure caused by increased respiratory effort and also due to likely disruption of the growth hormone-IGF 1 pathway.
This figure shows the improvement in weight percentile following adenotonsillectomy in a group of non-obese children with OSA. Girls are shown in panel A, boys in panel B.41 Note that these children had relatively mild OSA, with a mean obstructive apnea index of 6/hr, and SaO2 nadir of 85%. There was a decrease in work of breathing postoperatively, but no change in caloric intake.
37. Ahlqvist-Rastad J, Hultcrantz E, Melander H, Svanholm H. Body growth in relation to tonsillar enlargement and tonsillectomy. Int J Pediatr Otorhinolaryngol 1992;24(1):55-61.
38. Bar A, Tarasiuk A, Segev Y, Phillip M, Tal A. The effect of adenotonsillectomy on serum insulin-like growth factor-I and growth in children with obstructive sleep apnea syndrome. J Pediatr 1999;135(1):76-80.
39. Everett AD, Koch WC, Saulsbury FT. Failure to thrive due to obstructive sleep apnea. Clin Pediatr (Phila) 1987;26(2):90-2.
40. Freezer NJ, Bucens IK, Robertson CF. Obstructive sleep apnoea presenting as failure to thrive in infancy. J Paediatr Child Health 1995;31(3):172-5.
41. Marcus CL, Carroll JL, Koerner CB, Hamer A, Lutz J, Loughlin GM. Determinants of growth in children with the obstructive sleep apnea syndrome. J Pediatr 1994;125(4):
Girls
Boys
Marcus et al. J Pediatr 1994

48. NEUROCOGNITIVE MORBIDITY
Hyperactivity, inattention, aggression
Impaired school performance
Daytime sleepiness
Depression
The neurocognitive morbidity associated with pediatric OSA is likely to arise from sleep fragmentation and/or intermittent hypoxia. Studies from parental reports have documented that children with OSA have problems with inattention and hyperactivity, aggressiveness, daytime sleepiness and depression.34-36, 42-47
34. Gozal D, Pope DW, Jr. Snoring during early childhood and academic performance at ages thirteen to fourteen years. Pediatrics 2001;107(6):
35. Rosen CL, Storfer-Isser A, Taylor HG, Kirchner HL, Emancipator JL, Redline S. Increased Behavioral Morbidity in School-Aged Children With Sleep-Disordered Breathing. Pediatrics 2004;114(6):
36. Montgomery-Downs HE, Crabtree VM, Gozal D. Cognition, sleep and respiration in at-risk children treated for obstructive sleep apnea. European Respiratory Journal 2005;25(2):
42. Ali NJ, Pitson D, Stradling JR. Sleep disordered breathing: effects of adenotonsillectomy on behaviour and psychological functioning. Eur J Pediatr 1996;155(1):56-62.
43. Ali NJ, Pitson DJ, Stradling JR. Snoring, sleep disturbance, and behaviour in 4-5 year olds. Arch Dis Child 1993;68(3):360-6.
44. Chervin RD, Archbold KH, Dillon JE, et al. Inattention, hyperactivity, and symptoms of sleep-disordered breathing. Pediatrics 2002;109(3):
45. Chervin RD, Dillon JE, Bassetti C, Ganoczy DA, Pituch KJ. Symptoms of sleep disorders, inattention, and hyperactivity in children. Sleep 1997;20(12):
46. Gozal D. Sleep-disordered breathing and school performance in children. Pediatrics 1998;102(3 Pt 1):
47. Guilleminault C, Korobkin R, Winkle R. A review of 50 children with obstructive sleep apnea syndrome. Lung 1981;159(5):

49. CARDIOOVASCULAR MORBIDITY
Pulmonary Hypertension
Cor Pulmonale
Systemic Hypertension
Hypoxia during sleep is common in children with OSA; this can induce hypoxic pulmonary vasoconstriction which subsequently may lead to pulmonary hypertension and cor pulmonale.48 Diurnal elevation of diastolic blood pressure has also been reported in children with OSA.49
48. Stradling JR, Thomas G, Warley AR, Williams P, Freeland A. Effect of adenotonsillectomy on nocturnal hypoxaemia, sleep disturbance, and symptoms in snoring children. Lancet 1990;335(8684):
49. Marcus CL, Greene MG, Carroll JL. Blood pressure in children with obstructive sleep apnea. Am J Respir Crit Care Med 1998;157(4 Pt 1):

50. HYPERTENSION
Cohort of 700 children from kindergarten to 5th grade of the Dauphin County public school system in Hershey, Pennsylvania that underwent overnight PSG followed by detailed physical exam by otolaryngologist and pediatric pulmonologist. Suggest that AHI>5 should be threshold for treatment of SDB and AHI>3 should be threshold for closer monitoring of SDB. Snoring alone did not predispose to elevated BP but increased waist size was associated with increased SBP and this is suggestive of the metabolic syndrome.

51. HYPERTENSION
Systemic hypertension may occur in children with OSA. In this slide, the diastolic blood pressure index (the difference between the subject’s mean blood pressure during sleep and the blood pressure at the 95th percentile for age and height) is plotted against the apnea index. There is a significant correlation between the blood pressure index and apnea index.49
49. Marcus CL, Greene MG, Carroll JL. Blood pressure in children with obstructive sleep apnea. Am J Respir Crit Care Med 1998;157(4 Pt 1):
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