Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Anuj Chandra MD, D-ABSM Medical Director- Advanced Center for Sleep Disorders Adjunct Assistant Professor- University of Tennessee College of Medicine Chattanooga, TN Disclosures I have no financial relationships with commercial entities When is snoring concerning ? Habitual snoring: > 3 times/week without OSA “Benign” poor concentration, school performances History alone cannot differentiate habitual snoring from OSA When to treat snoring ? Obstructive Sleep Apnea (OSA) (American Thoracic Society) Disorder of breathing during sleep characterized by prolonged partial upper airway (Uaw) obstruction and/or intermittent complete obstruction (obstructive apneas) that disrupts normal ventilation during sleep and normal sleep patterns Sleep fragmentation Intermittent hypoxemia Intermittent hypercarbia OSA: Epidemiology Prevalence of snoring: 7-12% Prevalence of OSA Infants: 1 - 2% Children: 2 - 4% Adults: Women 2 - 4% Men 3 - 7% Snoring OSA OSA Lean 8 – 10% 2 – 3% Gender Prepubertal: M=F Post pubertal: M>F Peak incidence - 1.5 – 5 years (coincides with ATH) - Adolescence Obese 50% 36% 60% (metabolic syndrome) Risk factors for OSA Obesity Sickle cell disease Male Down syndrome African-American Prader Willi syndrome Prematurity Cranio-facial disorders Cigarette smoke exposure Neuromuscular disorders Adenotonsillar hypertrophy Cerebral palsy Asthma Allergic rhinitis Pediatric OSA: Overview Pathophysiology Anatomy Craniofacial size Soft tissues Fat distribution Ethnicity Neuromuscular Airway collapsibility Arousal threshold Ventilatory control Fluid shift Lung Volume Sleep OSA Thoracic pressure changes Sleep Fragmentation Hypercarbia Intermittent Hypoxia Gene trait, susceptibility Environment, diet, exercise Consequences Metabolic Cardiovascular Neurocognitive Autonomic Anatomical factors Craniofacial Factors/Syndromes Crouzon Apert Treacher Collins Hemi-hypoplasia Ziteli and Davis. Atlas of Pediatric Physical Diagnosis. 1997 Abnormal Dental Alignment Obesity & OSA: Partners in Crime ! Fatty infiltrates of UAw Risk of OSA in obese: Decrease lung compliance Odds ratio of 4.5 Increased resistive load ~ 36% - 55% have OSA Affect upper airway patency Post-T&A ~ 2/3rd have residual OSA OSA: Adverse Sequelae Individual genetic and environmental susceptible factors influences the ultimate expression of OSA sequelae…. OSA Cardiovascular Intermittent Hypoxemia Hypercarbia Sleep fragmentation Metabolic Respiratory Effort Insulin resistance Neuro-cognitive Dyslipidemia Endocrine BP dysregulation Endothelial Dysfunction EDS, ADD, poor memory Poor concentration Nocturnal Enuresis OSA:Neuro-behavioral consequences Hyperactivity/Inattentive Chervin et al, 2002; 109:449- Poor school performance Gozal et al, Pediatrics 1998: 102: 616- Aggressive behavior Gottlieb et al, Pediatrics 2003; 112:870- Excessive daytime sleepiness uncommon with AHI <20/hr Gozal et al, Pediatrics 2001; 108: 693- Cognitive deficits co-vary with endothelial dysfunction Gozal et al, Pediatrics 2010; 126; e1161- Diagnosis of OSA Evaluate symptoms and morbidity History, questionnaires Assessment for severity of obstruction Polysomnogram (Sleep Study) Assessment for site of obstruction: Clinical examination Radiological evaluation UA endoscopy Clinical features of OSAS Night time symptoms Snoring Daytime symptoms Excessive daytime Apneas Mouth breathing Choking or snorting arousals Paradoxical breathing Restless sleep Hyper-extended neck Frequent awakening Recent onset parasomnias sleepiness Morning headaches Mid-afternoon dip Hyperactivity Attention deficits Poor school performance Aggressive behaviors Chronic cough Physical Examination Weight Nose: BMI Deviated septum Neck circumference Turbinates Mouth Bite Tonsils Malampatti/Friedman Airway crowding Macroglossia Polyp Adenoids Face Mid-face hypoplasia Retro/micrognathia Allergic shiners Respiratory Cardiac: S2 and murmurr Staging of airways Friedman Classification Tonsils size Polysomnography (Sleep Study) EEG - For sleep stages EMG – for chin tone and leg movements EOG – eye movements Nasal pressure Airflow Oro-nasal thermister Chest and abdominal belts/summary – respiratory effort Oximetry with waveform Gas exchange ETCO2 with waveform Snoring microphone EKG - heart rate and rhythm Body position Video Grigg-Damberger et al, JCSM 2007: 3: 201 Indications for Sleep Studies Indications Respiratory Sleep related breathing disorders OSA Central sleep apnea Sleep Hypoventilation Periodic breathing Sleep hypoxemia Non-Respiratory Periodic limb movement of sleep (PLMS) Narcolepsy Nocturnal events seizures vs. parasomnia REM behavior disorders Not indicated Typical Parasomnias Insomnia Circadian rhythm sleep disorders Restless legs syndrome Obstructive apnea Severity of OSA Children Mild OSA AHI 1 – 5/hour Moderate OSA 5-10/hour Severe OSA > 10/hour Adults AHI > 5/hour with Symptoms AHI > 15/hour (without Sx) Mild: 5-15/hour Moderate: 15-30/hour Severe: > 30/hour Classification of OSA severity on PSG Principles and Practice of Pediatric Sleep Medicine 2nd Edn. 2014 Biomarkers of Pediatric OSA Helps with screening (urine, saliva, blood, exhaled breath) Early detection, cheap Bedside and can be done in clinic Follow up of response to medical or surgical intervention Potential biomarkers: Pediatrics: Combination of kallikrein-1, uromodulin, urocortin-3 and orosomucoid-1 appears to provide sufficient accuracy to be considered a potential OSA diagnostic test in children. Adults: IL- 6 and IL-10 appear to exhibit a favorable profile as biomarkers aiming to discriminate patients with and without OSA. Treatment of OSA in children Life style changes Weight loss: Diet, exercise Positional Alcohol avoidance Pharmacological treatment Inhaled steroids Leukotriene antagonist High flow nasal cannula Oxygen Surgical treatment Adenoidectomy Tonsillectomy Supraglottoplasty Positive airway pressure therapy CPAP Bi-PAP Pharmacological Treatment Effect of Intranasal Budesonide on OSA OAHI (/hr TST) Randomized double blind placebo controlled trial with the cross over design on children with mild OSA 13 PRE POST 13 12 12 11 11 10 10 9 9 8 8 7 7 6 6 5 5 4 4 3 3 2 2 1 1 0 0 0 5 10 15 20 25 30 35 40 45 50 Tx Group 0 62 recruited, 48 completed Budesonide or Placebo 6 weeks on treatment 2 week washout 6 weeks other treatment 5 10 15 20 25 30 Control Kheirandish-Gozal et al, Pediatrics 2008 Anti-inflammatory therapy outcomes for mild OSA Retrospective analysis 2-14 years old 2007 – 2012 Mild OSA Combination ICS and oral montelukast x 12 weeks N = 3027, 836 fulfilled criteria, 752 received Rx Overall beneficial effect > 80% Normalization of PSG 62% (17% no change) Non responders: age > 7 years and obesity Kheirandish-Gozal Chest 2014 Adeno-tonsillectomy First line of therapy Recent data: 25-60% have residual OSA Discrepancy between tonsillar size & OSA severity No consensus AHI cut-off to perform T&A Adenoidectomy alone: 30% likely for 2nd surgery within 3 yr2 Complications: pain, bleeding and death 1. Guilleminault et al. J Pedriatr 1989 2. Brietzke, Katz and Roberson et al: Int J Ped Otorhinol 2006 Washtenaw County Adenotonsillectomy Cohort Giordani et al, J Int Neuropsych Soc 2012; 18: 212- Follow-up at 1 year: Sleep Variables Apnea Index Subjective Sleepiness MSLT OSA (n=40) 5.6 0.1 49% rare 15.6 17.5 Snoring (n=38) 0.2 0.1 27% rare 15.9 17.3 17.4 17.3 Surgical Controls (n=27) 0.1 Rare Improvement over time. No Differences at Follow-up vs. Controls High Risk Groups for Residual OSA after T&A Older children: > 7 years Obese children Severe baseline OSA Syndromic patients: Down syndrome, Prader Willi, Craniofacial syndromes (Treacher Collins, Pierre Robin) Neuromuscular disorders: hypotonia, cerebral palsy Significant Allergies and Asthma Orthodontic disorders 12 obese children BMI ~ 35 Age: 10 years Range of AHI: 2-36/hour High flow nasal cannula (20 L/min) room air 2 PSGs: on and off Nasal cannula High flow NC group: AHI reduction: 11+3 to 5+2 per hour) P<0.001 EEG arousal, RR, desaturation were also noted Pediatrics 2009 Positive airway pressure therapy First described use in OSA in 1981 Considered the "gold standard" of therapy Treatment, not cure Stents UAw open, preventing dynamic collapse Increases FRC, pulmonary reserve Indications Residual OSA Surgery contraindicated Hypoventilation Pediatric CPAP mask Resmed Infant Bubble Mask Pixie nasal mask Respironics Petit Gel Full Face Mask Mini Me 2 Pixie nasal mask Other upper airway surgeres NASAL CAVITY Septoplasty, Turbinate reduction NASOPHARYNX Revision adenoidectomy PALATE and OROPHARYNX Uvulopalatopharyngoplasty (UPPP)/ Expansion pharyngoplasty ORAL CAVITY Tongue reduction HYPOPHARYNX Lingual tonsillectomy, Tongue base reduction / Glossoptosis procedures LARYNX Supraglottoplasty, dilatation of subglottic stenosis Rapid maxillary expanders: Increase in the width of the palate, nasal cavity, corrects deviated septum Age 5-13 years Mandibular repositioning devices Role of Bariatric Surgery in Adolescence Failed clinical treatment with multidisciplinary and adequate therapy Body Mass Index: BMI > 40 kg/m2 with comorbidities (DM2, HTN, dyslipidemia) BMI > 50 kg/m2 without comorbidities Good comprehension and cognition to follow all necessary procedures before and after surgery Not pregnant in year before surgery Good family support. Bariatric surgery Most centers: Age >16 years Roux-en-Y gastric bypass & adjustable gastric ban Sleeve gastrostomy Kalra et al 2005 34 obese adolescents 19 patients had AHI > 5/hour 10 had repeat sleep study After significant weight loss (mean, 58 kg), OSA severity markedly decreased in all patients Baseline median AHI vs. after weight loss = 9.1 vs. 0.65 per hr Take home messages OSA is very common in children, but under recognized & under treated Carries many short & long term health risks, some of which are unique to children and may be irreversible Consider medical management for mild OSA Although A&T is effective, recent data shows increasing number of children with residual OSA despite surgery Consider referral to pediatric sleep specialist when indicated 41 American Academy of Pediatrics: Guidelines for Pediatric OSA 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 Pediatrics 2002;109:704 Childhood Parasomnias Undesirable events or experiences occurring: At entry into sleep Within sleep During arousal from sleep Parasomnia Classification Disorders of Arousal (from NREM sleep) Parasomnias Associated with REM Sleep Other Parasomnias Sleep Terrors • • • • Peak age: 5-7 years Prevalence rate of 2.0 - 6.5% Most will later sleepwalk Usual duration in children:- 4 years – 50% end by age 8 – 36% continue into adolescence Sleep Terrors • • • • Begin abruptly from NREM sleep Episodes of agitation and apparent terror Heralded by a blood-curdling scream or cry Followed by confusion, agitation and autonomic disturbances • Patient difficult to arouse • If patient can be awakened, may describe: – Vague sense of terror – Isolated or fragmented dream imagery Parasomnias Associated with REM Sleep • Nightmares • Sleep paralysis • REM Sleep Behavior Disorder Nightmares 75% of children experience nightmares 10 - 50% of children have nightmares severe enough to disturb their parents Proportion of children reporting nightmares reaches a peak around ages 6-10 years and decreases thereafter Nightmares: Clinical Characteristics • Usually during last half of night • Complex dream mentation: - “Good dream gone bad” • Emotional reaction more significant than autonomic response • Fully alert upon awakening • Responsive to comforting Nightmares: Precipitating Factors • Anxiety / Stress • Personality – association with creativity • Post-traumatic stress disorder Nightmares: Treatment • Explanation and reassurance • Sleep hygiene • Behavioral therapies Nightmares vs Sleep Terrors Nightmares • • • • • • • • REM sleep Most common parasomnia Second half of night Delayed return to sleep Easily comforted Detailed narrative description of episode Mild autonomic activity Alert upon awakening Sleep Terrors • • • • • • • • NREM sleep 2.0 - 6.5% prevalence First half of night Rapid return to sleep Resists comforting Fragmented recall / amnesia Intense autonomic activity Confusion on waking Enuresis: Definition Persistent bedwetting more than twice a month past the age of five years Primary enuresis: Patient has never been dry on a regular basis Secondary enuresis: Patient becomes enuretic after being dry for at least six months Enuresis: Declines with Age Enuresis: Theories Plasma Vasopressin (pg/ml) 4 3 2 1 0 8:00 AM 12 Noon 4:00 PM 8:00 PM Normals 12 Mid 4:00 AM 8:00 AM Enuretics Enuresis: Other Theories Functionally small bladder capacity Dysfunctional detrusor activity Higher arousal threshold Percentage of Children with Frequent Enuresis Enuresis and Pediatric OSA 60 Obstructive sleep apnea should be considered in the differential diagnosis of enuresis in children 50 40 Frequent enuresis is 30 more common in children with a higher apnea hypopnea index (AHI) 20 10 0 AHI < 1 AHI > 1 Enuresis: Evaluation History Developmental milestones Family history Physical / neurological exam Urinalysis Evaluation of urinary stream and bladder capacity Enuresis: Behavioral Treatment Limit fluids / caffeine near bedtime Positive reinforcement Hypnosis and imagery Bladder stretching Sphincter training Scheduled wakings Urine alarms Enuresis: Pharmacologic Rx DDAVP (Desmopressin) Effective in most patients Tablets and nasal spray Low frequency of side effects: Concern for diabetes insipidus Hyponatremia Imipramine ECG abnormalities Possible behavior problems Disorders of Arousal Arousals from NREM sleep First half of night, typically short duration Prolonged or multiple episodes may occur Confusion / automatic behavior Difficult to awaken during event Fragmented imagery Rapid return to sleep after event Amnesia of events Disorders of Arousal Abrupt Arousal Partial or complete arousal from sleep Confusional Arousals: Clinical Characteristics • • • • Occur on arousal from NREM sleep May not recognize parents May cry, yell, or moan Speech often unintelligible, sounds like words • Most common words: “No, No!” Sleepwalking: Clinical Characteristics • Quiet wandering (injury unlikely) • Agitated wandering (injury more likely) • Behaviors of variable complexity • Inappropriate behaviors • Most sleepwalkers have few daytime effects Disorders of Arousal: Familial Basis – 60% of children have positive family history – 10-fold increased prevalence in first-degree relatives of an affected individual Disorders of Arousal: Evaluation Video-PSG needed if: – Spells have atypical features – Spells are stereotyped – Patients describe potentially injurious behavior or have injured themselves or others PSG needed if OSA is suspected Disorders of Arousal: Treatment Allow episodes to run their course: Interfere only to prevent injury May try to lead the patient calmly to bed Emphasize sleep hygiene Secure the bedroom to prevent injury: Consider ground floor bedrooms Window and door locks, pad bedrails Remove sharp objects or toys on bedroom floor Alarms or barriers at door/stairs Medications may be necessary in severe cases Pediatric RLS An urge to move legs, caused by discomfort as described in child’s own words Begins or worsens during periods of inactivity Partially or totally relieved by movement Worse in the evening or night Biological parent / sibling with definite RLS Periodic limb movements of five or more per hour of sleep on PSG Pediatric RLS: Clinical Features Attention sought for “growing pains” These present as: Sleep onset problems Sleep maintenance problems Daytime irritability and attention problems may occur, likely due to sleep deprivation Family history is positive for RLS Iron deficiency may play a role as in adults Pediatric RLS: Prevalence “Night-Walkers” Survey 138 adults with RLS (mean age 60 years) 18% reported symptoms began before age 10 years 25% reported symptoms began before age 20 years Childhood RLS case reports Walters AS. Neurology 1996;46:92 Pediatric RLS: Treatment Strict sleep hygiene is necessary to avoid sleep deprivation Limiting setting often required (day and at bedtime) Treatment of iron deficiency Medications: Clonazepam 0.25 to 1.0 mg qHS Insomnia Complaint of: Difficulty initiating sleep (bedtime resistance) Maintaining sleep (inability to sleep independently) Daytime impairment: Inattention, mood disturbance Problems with memory and concentration Impaired performance (at school in children) Behavioral Insomnia of Childhood Symptoms meet criteria of insomnia Pattern consistent with either: Sleep-onset association type Limit-setting type Behavioral Insomnia of Childhood Evaluation History Precise description of the problem Parent response and interaction with child Typical night, not extremes Careful description of bedtime routines, including naps Evaluate the 24-hour schedule (weekday, weekend, vacation) Behavioral Insomnia of Childhood: Sleep-onset Association Type • • Child begins to associate sleep onset with circumstances that are problematic and demanding of the caregiver. Child is unable to fall asleep without these associations either at initial sleep onset or during nocturnal awakenings. Treatments for Sleep-onset Association Type Education Awakenings during the night are normal Sleep onset associations are learned Sleep onset associations are present at all ages New sleep onset associations can be taught Behavioral treatment • • • • • • Place child in crib/bed awake and leave room If child is upset, return to comfort Do not pick up the child; comfort verbally Stay in room briefly, leave before child sleeps Increase time between responses Same routine for awakenings and naps Treatments for Sleep-onset Association Type • Usual response between three to five nights • If symptoms persist, consider: – – – – – Instructions not followed Co-existing problems Error in diagnosis More time needed Modifying the technique • Modified techniques: – Eliminate associations in stages – Parents present longer – Limit physical contact – Gradually withdraw Behavioral Insomnia of Childhood: Limit-setting Type • • Refusal to go to bed at an appropriate time or following a nighttime awakening Insufficient or inappropriate limit setting demonstrated by the caregiver Behavioral Insomnia of Childhood Limit-setting Type: Favorite Delay Tactics “Mommy …” “Daddy, I need…” I’m hot. I’m cold. I’m scared. I’m not sleepy. I’m thirsty. My tummy hurts. I hear something. I have to go to the bathroom. Fix my blanket. I need to be tucked in again. A drink. One more kiss. One more hug. The light on. The light off. To tell you something A band-aid. My mommy. You to cover me up. You to rub my back. A tissue. Some medicine Behavioral Insomnia of Childhood: Limit-setting Type • • • Bedtime refusals, stalling and repeated demands May also occur at naptime and nighttime awakenings May be straightforward or complex Treatment of Limit-setting Type Emphasize the importance of limit-setting Teach general limit-setting guidelines (day as well as night) Specific and individualized techniques (gate, progressive door closure) Positive reinforcement (star chart) Thank you 85