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Evaluation and Management of Sleep Disordered Breathing PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Evaluation and Management of Sleep Disordered Breathing" by Kathy Shelly, PA-C.

This medical PowerPoint presentation is about sleep-disordered breathing (SDB), a condition in which a person has difficulty breathing during sleep. It is a common disorder that affects a large number of people and can cause a range of health problems, including sleepiness during the day, snoring, and other issues.

The evaluation and management of sleep-disordered breathing typically involve a multi-disciplinary team, including a sleep specialist, pulmonologist, and/or ENT surgeon.

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Published on : Jun 23, 2023 | Views : 1334 | Downloads : 3

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Evaluation and Management of Sleep Disordered Breathing Kathy Shelly, PA-C Texas Children’s Hospital Department of Surgery: Otolaryngology
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Learning Objectives Review the anatomy of the pediatric nasopharyngeal and oropharyngeal cavity Analyze information obtained from PSG and the indications for surgical and medical management of SDB Recognize typical adenotonsillectomy recovery expectations
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What is Sleep Disordered Breathing? Sleep disordered breathing (SDB) is a general term for breathing difficulties occurring during sleep. This can range from primary snoring and mouth breathing all the way up to obstructive sleep apnea (OSA). There are many other types of sleep issues that may not have anything to do with breathing issues.
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10% of children snore regularly. Snoring alone can disturb the sleep pattern depriving the snorer of adequate rest. However, when the breathing is disrupted, the body perceives this as a choking event and results in the following physiological ways: the heart rate slows the blood pressure rises the brain is aroused sleep is interrupted the oxygen level in the blood may drop increasing the work of the heart.
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Sleep Disordered Breathing
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The disruption of the normal sleep cycle can make one feel poorly despite spending an adequate amount of time in bed. The snorer stays in a lighter phase of sleep to keep the throat muscles more tense in order to keep the airflow to the lungs open. In adults, this has been well studied, and this has been shown to affect daytime sleepiness/somnolence, complaint of fatigue and job performance. It is more dangerous to drive and operate heavy equipment. There is an increased risk of having an MI, CVA, diabetes and one is more likely to be involved in a MVA. In children, the are noted to have fewer cortical arousals and preservation of the sleep architecture but varied manifestations of sleepiness.
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Potential Consequences of untreated SDB/OSA behavior/learning – a hallmark of adult OSA is excessive daytime somnolence/sleepiness. This is common in adolescents also, but children may have issues with being moody/grumpy, hyperactive, inattentive, impaired learning and diminished academic performance, aggressive becoming disruptive both at home and at school. They may also be more likely to have sleep walking and night terrors. cardiovascular – long term, can be associated with an increased risk of high blood pressure or right ventricular dysfunction and elevated pulmonary arterial pressure growth – secondary to impaired growth hormone secretion, there is a higher risk of failure to thrive and impairment of growth development
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obesity – SDB may cause the body to have increased resistance to insulin contributing to obesity and daytime fatigue may decrease physical activity participation social – loud snoring can become a significant problem if the child shares a room with sibling(s) or is at a sleepover/summer camp enuresis – SDB can cause increased night time urine production from decreased release of anti-diuretic hormone
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Often times, the diagnosis of sleep disordered breathing can be made based on parental history only and is then supported by the physical exam. In special cases, such as in a child with a craniofacial syndrome, morbid obesity, sickle cell disease, seizures or a neuromuscular disorder and for children less than 3 years of age, additional testing may be recommended.
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Overweight children are at an increased risk for SDB because of the fat deposits around the neck and throat narrowing the airway. Extra weight on the frame interferes with the ability of the chest and abdomen to fully expand during breathing hindering the intake of air and increasing the risk of sleep apnea. Overweight is anyone with a BMI of 25 or above. Obesity is having a BMI of 30 or above. Morbid obesity is a BMI of 40 or above with “morbid” indicating that the risk of obesity related illness is increased dramatically at this degree of obesity.
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What is OSA? Obstructive Sleep Apnea (OSA) is a condition involving repeated episodes of partial or complete blockage of the airway during sleep as detected by a polysomnography (PSG, also referred to as a sleep study or SS). There are other types of sleep issues that may be diagnosed by PSG not associated with obstruction. The prevalence of OSA is estimated to be between 1-4% in preschool and school-aged children. Recently, the estimated prevalence has increased due to better monitoring techniques during PSG.
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OSA viscous cycle
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So, what exactly are the tonsils and adenoids? The tonsils and adenoids are similar to the lymph nodes/glands found in the neck, groin and armpits. The tonsils are the 2 round lumps located in the back of the throat and they are enclosed in a fibrous capsule. Adenoids are high in the throat at the very back of the nose and are not visible on typical exam with out the use of special instruments. The 2 most common issues with the tonsils and adenoids is infections and enlargement. The adenoids may be enlarged producing mouth breathing and a chronic runny nose. Recurrent sinusitis and recurrent ear infections are also common.
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In order to understand how adenotonsillar hypertrophy(ATH) can impact SDB/OSA in children, a review of the pediatric airway anatomy and how the airway is affected during SDB/OSA is important to understand. The disorder is most common between the ages of 2-10 years of age and correlates to the age of lymphoid hyperplasia during childhood.
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Blood supply of the tonsil
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Nasal Obstruction – Adenoid Hypertrophy
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Turbinate Hypertrophy
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Nasal Polyps
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Tonsil Grading
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Mallampati Score Mallampati score – this is an anestheisology assessment of the “crowdedness” of the oral airway
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Sleepy Kids = Sleepy Parents
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Describe events from dinner time until sleep onset Is their a a set bedtime? Is it developmentally appropriate? Is it consistent from night to night? Is it enforced? What are the child’s evening activities? Heavy meals not w/in 1-2 hours before bedtime? Any high energy activities w/in hour before bedtime? Is there a bedtime routine? Are there any sleep associations present? What is happening at sleep onset? Where is it occurring? Any bedtime refusal? History: Bedtime behaviors
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What is happening at the time child is falling asleep? What is the time from lights out to sleep onset? > 20 minutes indicates difficulty falling asleep Asking the child/adolescent directly is important Sleep anxiety? Restless leg syndrome symptoms? What is the level of sleepiness? Does the child really feel sleepy at a later bedtime indicating a possible delayed phase in circadian rhythm? Where is sleep onset occurring and is there then transfer after sleep onset? Is the location of sleep onset variable? Does the child fall asleep on the couch watching TV and is then moved? Falling asleep
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Bedroom and bed location Bedroom or bed sharing may increase night wakenings If location of child’s bedroom far from parents room may increase child’s anxiety Light May interfere with melatonin secretion Need for bright light may be indicative of anxiety issues Bed type Moving a child from crib to bed prematurely may exacerbate sleep problems Bedding No data on advantage of different sleeping surfaces and sleep quality Infants who sleep on soft surfaces are at increased risk for suffocation and SIDS Sleep Environment
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Is it difficult to wake the patient in the morning? Does it take multiple attempts? When would the child spontaneously wake if allowed? Best elicited during vacation or summer days Helps determine their preferred time of sleep and average sleep need. Difficulty waking despite seemingly adequate amount of sleep may indicate the quality of sleep is affected Are there consequences to difficulty waking? Habitual tardiness Morning awakening
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Indicative of significant daytime sleepiness Morning waking difficulties Daytime sleepiness Fatigue Daytime dysfunction Presence of unplanned napping at all ages and the need for planned naps in a child after 5-6 years of age is suggestive of insufficient sleep and/or poor quality sleep. Daytime behaviors
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A brief Sleep screening tool for sleep - BEARS Mindel, JA, & Owens, JA. (2003) A Clinical Guide to Pediatric Sleep: Diagnosis and Management of Sleep Problems. Lippincott, Williams & Wilkins. Philadelphia, PA.
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Consistent and Positive Routines Keep the same exact routine every night Use a regular series of positive, relaxing behaviors and interactions that replace frustration and conflict prior to sleep: Sleep in the same place every night Engage in relaxing nighttime activities Go to bed and get up at the same time No caffeine after lunch Create a dark, cool sleep environment Take away the clock Avoid daytime napping Useful at all ages
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History, continued Medical Hx GERD; seizures; allergies/eczema/asthma Developmental Hx Repeating a grade in school Any other developmental delays Academic Hx Repeating a grade in school Familial Factors Genetics; culture; conflicts Psychiatric/Behavioral Hx Anxiety; mood; inattention; making friends
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Family functioning Effectiveness of parenting Family schedule Shift work Psychologic status of parent Parental divorce Discrepancies in parenting styles Consistency of sleep patterns at 2 different households Significant life events Moving to own room Family culture How are the child’s sleep problems impacting the family? Is the parent having daytime dysfunction? Falling asleep while driving Psychosocial History
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20-30% of children have sleep problems at some time during their life. In the neurologically/developmentally challenged children, this increases to 40-100%. “Good sleep” has to do with the timing and the amount of sleep in addition to the continuity of sleep.
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Sleep Requirements of Typically Developing Children 0-2 months: 16-20 h; no night/day pattern 2-12 months: 9-12 h; 4-1 naps (2-5h) 1-3 yr: 12-13 h per 24 h; 2-1 naps 3-5 yr: 11-12 h per 24 hr; 1-0 naps 6-12 yr: 10-11 h; 0 naps 12-18 yr: 9-9.5 hr; 0 naps
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Difficulty Sleeping Poor sleep hygiene, OSA, RLS, PLMD, Parasomnias, Circadian Rhythm Disorders Excessive Sleepiness Insufficient Sleep, Circadian Rhythm Disorders, Narcolepsy, Hypersomnia
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Caregivers may be less attuned to sleep issues beyond the early childhood period. Some caregivers may not regard some symptoms as problematic Often differences between child and parent perspective Not uncommon for parents to say that their child has “never slept well” Other challenges
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Sleep and Anxiety Center for Kids SACK is a clinical research center in the Department of Psychology at the University of Houston offering research opportunities and low-cost treatment services for children based on the latest scientific evidence. U.S. military families services are offered services at no charge. 4505 Cullen Blvd.Houston, TX 77204Phone: 713-743-3400Fax: 713-743-8633Email: SACK@uh.edu
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Physical exam is normal in many children with sleep disorders Growth parameters FTT and obesity are both associated with SDB/OSA Tanner stage in patient with recent onset sleep initiation insomnia Onset of puberty is associated with normal biological shift in sleep-wake cycles Do they fall asleep during the examination or are they hyperactive/irritable/dis-inhibited Significant sleep disruption or inability to self soothe may be an early indication of developmental delay Physical Exam
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Otolaryngologic examination Assessing for risk factors for OSA Tonsillar hypertrophy Narrowed/small oropharynx Nasal congestion Neurologic exam Concern for excessive sleepiness or nocturnal seizures Brainstem dysfunction if suspecting central sleep apnea Abnormal sensation if suspecting secondary restless leg syndrome Physical Exam
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A couple of key points Large tonsils and adenoids does not always indicate the presence of OSA Loudness of snoring does not correlate with degree of OSA A formal sleep study remains the gold standard in diagnosing OSA and other sleep related disorders.
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Polysomnography (PSG) orSleep Study (SS) This is an objective test in which wires are attached to the head and body that monitor brain waves, muscle tension, eye movement, breathing and level of oxygen in the blood. The test is not painful and is generally performed in a sleep lab or hospital. The role of PSG includes the following: Meet diagnostic criteria of pediatric OSA according to ICSD 2 Differentiate OSA from primary snoring Define severity of OSAS Evaluate excessive daytime sleepiness (i.e. narcolepsy) Evaluate for periodic limb movement disorder Evaluate success of treatment
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Clinical Practice Guidelines PSG for SDB prior to tonsillectomy in children 2-18 years of age – improving referral patterns for PSG: Complex medical conditions such as obesity, Down syndrome, craniofacial abnormalities, neuromuscular disorders and sickle cell disease. When there is discordance between tonsillar size on physical exam and reported severity of breathing. Results of PSG should be communicated to the anesthesiologist prior to the induction of anesthesia. Children admitted with OSA younger than 3 years of age or if severe AHI or 10 or more obstructive events per hour or with an O2 nadir <80%.
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Courtesy of Dr. Carol Rosen 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
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 sleep onset latency  wake after sleep onset  sleep efficiency  REM latency  amount of REM sleep No significant difference in NREM sleep Despite the first-night effect, the diagnosis of Obstructive Sleep Apnea in children can usually be reliably confirmed by one night of PSG “First-night Effect” with PSG
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Obstructive Apnea 2 missed breaths > 90% fall in signal amplitude Continued respiratory effort Duration: Last normal breath to the beginning of the first breath that achieves the pre-event baseline inspiratory excursion
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Mixed Apnea 2 missed breaths > 90% fall in signal amplitude No inspiratory effort initially, but toward end of the event, the effort returns
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Central Apnea Absent inspiratory effort throughout event 1 of the following Lasts longer than 20 seconds Lasts at least 2 missed breaths and is associated with an arousal, awakening, or a > 3% desaturation.
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Obstructive Hypopnea > 50% drop in amplitude of the nasal pressure 2 breaths Associated with Arousal Awakening >3% desaturation
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Respiratory Effort Related Arousal (RERA) Nasal pressure sensor Must meet following criteria < 50% decrease in amplitude Flattening of the wave form Assoc with snoring, noisy breathing, increased pCO2, or increased work of breathing Lasts 2 breaths Associated with arousal
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Hypoventilation > 25% of the total sleep time has pCO2 > 50mmHg Can be prominent in patients with neuromuscular disease Concern for underlying cardiopulmonary factors
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Apnea/Hypopnea Index (Obstructive Apneas + Central Apneas Mixed Apneas + Hypopneas) per hour of sleep. Mild >1 to 5 Moderate >5 to 15 Severe = > 15
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Respiratory Disturbance Index (Obstructive Apneas + Central Apneas Mixed Apneas + Hypopneas +RERAs) per hour of sleep. Mild >1 to 10 Moderate >10 to 20 Severe >20
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RESPIRATORY ANALYSIS: The patient was recorded while sleeping in the supine, prone, and side positions. Snoring was recorded. During wakefulness the respiratory rate was 12-14 breaths per minute. During sleep the respiratory rate was 12-18 breaths per minute. The baseline oxygen saturation was 99%. The oxygen nadir was 74%. The patient spent 1.3% of the total sleep time with oxygen saturation values less than 90%. The transcutaneous pCO2 values were elevated to as high as 51 mmHg. During 1.6% of the monitoring time pCO2 values were elevated above 50 mmHg (significant values > 25%). During sleep, 9 obstructive apneas, 1 mixed apneas, 6 central apneas (8.7-15.3 seconds), 110 obstructive hypopneas, and 13 RERAs were recorded. The apnea hypopnea index was 16.60. The obstructive apnea hypopnea index was 15.81. The respiratory disturbance index was 18.31 (17.52 obstructive respiratory events per hour of sleep). Respiratory events were more frequent during REM sleep (44.42 respiratory events per hour of REM sleep). Of note, there were intermittent episodes of thoracoabdominal asynchrony. CARDIAC ANALYSIS: The heart rate was typically in the range of 69-113 beats per minute. No significant cardiac arrhythmias were recorded. LIMB MOVEMENT ANALYSIS: During sleep, there were 0.0 periodic limb movements recorded (0.0 per hour of sleep; significant values greater than 5.0 per hour of sleep). EEG CHARACTERISTICS: The occipital dominant rhythm was 7-8 Hz. There were no focal or lateralizing features. No epileptiform abnormalities were recorded. IMPRESSION: During this sleep evaluation, severe obstructive sleep apnea (17.52 obstructive events per hour of sleep and snoring) was recorded. Respiratory events were more frequent during REM sleep (44.42 respiratory events per hour of REM sleep). The minimum oxygen value was 74%; pCO2 values were mildly elevated but did not meet the criteria for sleep related hypoventilation. ECG and EEG findings were normal on this overnight sleep evaluation. RECOMMENDATIONS: 1. Evaluation of the upper airway for anatomic abnormalities, including chronic nasal congestion, is recommended. 2. If the patient undergoes surgery, then a follow up study in 6-8 weeks after surgery is recommended. 3. If the patient is not a surgical candidate and has significant daytime impairment, then other therapeutic options include a trial of positive airway pressure (PAP). This would require a second night titration study. 4. Repeat sleep study in 12 months is recommended, sooner if clinically indicated, in order to reassess the severity of sleep disordered breathing.
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RESPIRATORY ANALYSIS: The patient was recorded while sleeping on the back and sides. Minimal snoring was recorded. During wakefulness the respiratory rate was 17-25 breaths per minute. During sleep the respiratory rate was 16-26 breaths per minute. The baseline oxygen saturation was 98%. The oxygen nadir was 93%. The patient spent 0% of the total sleep time with oxygen saturation values less than 90%. The transcutaneous pCO2 values were elevated to as high as 42mmHg. During 0% of the monitoring time pCO2 values were elevated above 50 mmHg (significant values > 25%). During sleep, 0 obstructive apneas, 0 mixed apneas, 3 central apneas (8.9-10.2 seconds), 3 obstructive hypopneas, and 18 RERAs were recorded. The apnea hypopnea index was 0.72. The obstructive apnea hypopnea index was 0.36. The respiratory disturbance index was 2.87 (2.51 obstructive respiratory events per hour of sleep). Respiratory events were more frequent during REM sleep (4.94 respiratory events per hour of REM sleep). CARDIAC ANALYSIS: The heart rate was typically in the range of 53-120 beats per minute. Rare PVCs were recorded. In addition, there were intermittent episodes of elevation of the ST segment. Of note, there was a significant amount of ECG artifact. LIMB MOVEMENT ANALYSIS: During sleep, there were 0.0 periodic limb movements recorded (0.0 per hour of sleep; significant values greater than 5.0 per hour of sleep).EEG CHARACTERISTICS: The occipital dominant rhythm was 7-8 Hz. There were no focal or lateralizing features. No epileptiform abnormalities were recorded. Few episodes of bruxism was recorded. IMPRESSION:This patient was previously diagnosed with mild OSA on 4/2013. The current study was performed to reassess the severity of sleep disordered breathing. During this sleep evaluation, mild obstructive sleep apnea (2.51obstructive events per hour of sleep and snoring) was recorded. The minimum oxygen value was 93%; pCO2 values were not significantly elevated.ECG findings were abnormal (rare PVCS, ST segment elevation); however, there was a significant amount of artifact on the single lead EKG monitor. EEG findings were normal on this overnight sleep evaluation. Few episodes of bruxism was recorded. RECOMMENDATIONS:1. Evaluation of the upper airway for anatomic abnormalities, including chronic nasal congestion, is recommended. 2. If the patient undergoes surgery, then a follow up study in 6-8 weeks after surgery is recommended.3. If the patient is not a surgical candidate and has significant daytime impairment, then other therapeutic options include a trial of positive airway pressure (PAP). This would require a second night titration study. 4. ECG showed rare PVCs and intermittent episodes of ST segment elevation in the setting of significant amounts of artifact. This was recorded on a one lead EKG monitor. Clinical correlation and/or follow up with a 12 lead EKG is strongly recommended. 5. For the bruxism, dental evaluation is recommended. 6. Repeat sleep study in 12 months is recommended, sooner if clinically indicated, in order to reassess the severity of sleep disordered breathing.
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Treatment for SDB/OSA 1st line treatment is adenotonsillectomy (T&A). Of the over 500,000 pediatric T&As performed in the US each year, the majority are done to treat SDB. Many children with SDB/OSA show both short and long term improvement in their sleep after T&A but not EVERY child with snoring should undergo T&A as the procedure does have risks. If the SDB/OSA is mild or intermittent, academic performance and behavior are not concerns, the tonsils are small, or the child is near puberty, it may be recommended that they should be conservatively monitored.
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Tonsillectomy indications for OSA T&A is typically performed on an out-patient basis. The procedure takes about 35-45 minutes and is performed under general anesthesia. Post-operative observation lasts for several hours, but children under the age or 3 years of age, those that have severe OSA per sleep study and those with other medical issues are typically kept overnight for monitoring of their respiratory status.
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Types of T&As Coblation (involves using cool electrical current to remove tonsillar tissue; may produce less postoperative pain and a faster recovery) Dissection (most common method; involves removing the tonsils using a scalpel) Electrocauterization (involves using hot electrical current to remove the tonsils; may cause damage to surrounding tissue that increases postoperative pain) Harmonic scalpel (involves using a scalpel that vibrates; minimizes bleeding and damage to surrounding tissue)
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Laser ablation (involves using a hand-held laser to vaporize tonsillar tissue) Microdebridement (involves using a rotary "shaving" device to remove tissue from enlarged tonsils Radiofrequency ablation (also called somnoplasty; involves using energy transferred through probes inserted into the tonsils) Types of T&As (contined)
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Partial tonsillectomy (intracapsular tonsillectomy) with the use of power instruments that produce radiofrequency energy or coblation or laser has been advocated because the procedure has been shown to result in less post-op pain and an earlier return to normal diet and daily activity. The capsule is not disturbed therefore the underlying muscle is not encountered. 3.2% of children who underwent this technique experienced tonsillar regrowth and recurrence of snoring during a 2 year period following the first procedure. Types of T&As (contined)
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Recovery after T&A Average recovery is 7-10 days. Post-operative problems: swallowing, vomiting, fever, throat/ear pain, bleeding from the nose/mouth. Drinking is the most important part of recovery and starts immediately after surgery. Dehydration is a common issue for children in the post-operative period. Eating is typically a soft diet but the sooner the child eats/chews, the quicker the recovery. Weight loss during the recovery is not uncommon.
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Recovery after T&A A low grade fever may be observed the first night after surgery and even continue for a day or 2 but the surgeon’s office should be contacted if it is greater than 101.0° F. Nearly all children will have mild to severe throat pain after surgery. Ear pain, stiff neck or jaw pain are also frequently reported. The type of pain medication has changed since the findings regarding codeine metabolism. Rectal suppositories and liquid medications are recommended instead of tablets/capsules and pills.
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Activity may be increased slowly with a return to school after a return to normal eating and drinking and pain medications are no longer required and the child is back to sleeping through the night. Snoring and mouth breathing due to the swelling in the throat is not uncommon during the recovery period but should subside within 10-14 days after the procedure. Scabs look like thick, white discharge and causes bad breath and is often mistaken as an infection. Most scabs will fall off in small pieces 5-10 days after surgery. Bleeding of bright red blood should not be seen. Recovery after T&A
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ImmediatePost Tonsillectomy Complications Hemorrhage Protracted vomiting Severe Pain Decreased PO Intake/Dehydration Postoperative pulmonary edema Postoperative airway obstruction
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DelayedPost Tonsillectomy Complications Hemorrhage (post 24 hours) NP/choanal stenosis Pharyngeal stenosis Velopharyngeal insufficiency Grisel’s syndrome (atlantoaxial subluxation)
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Postoperative bleeding risk factors The UK National Prospective Tonsillectomy Audit demonstrated that there was a higher risk of postoperative bleeding with: Increasing patient age Male gender History of recurrent acute tonsillitis (3.7%) Previous peritonsillar abscess Rate for quinsy patients (5.4%) compared with patients with pharyngeal obstruction and OSA (1.4%) Primary hemorrhage range from 0.2% to 2.2% of patients. Secondary hemorrhage 0.1% to 3%.
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T&A Outcomes T&A results in significant improvement in the QOL based on validated questionaires measuring sleep disturbance, physical and emotional symptoms, hyperactivity and daytime functioning. Pulmonary HTN has normalized based on ECHO assessment. School performance is improved. Health care utilization is reduced. Abnl PSG measurement including respiratory disturbance index (RDI), oxygen saturation and arousal index have resolved. However, many children continue to have residual SDB/OSA after surgery. Factors contributing to residual sleep concerns include the severity of OSA prior to T&A, obesity, +FH as well as African American descent. Untreated nasal obstruction and maxillofacial deformity contributing to diminished airway dimension are also frequent findings in those inadequately treated by T&A. Additional surgery may be warranted such as jaw expansion by orthodontics, maxillofacial surgery or nasal airway reconstruction. Some children will benefit from PAP titration. Tracheotomy is reserved for the most severe of cases.
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Tracheotomy Bypasses areas of airway obstruction during sleep Generally reserved for most severe cases of OSA Patient refractory to other therapies
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Risk Factors for persistent OSA after T&A Obesity Older age at time of surgery (varies per article >7 y/o) More severe sleep apnea preoperatively Asthma in nonobese children Craniofacial & mandibular anomalies Cerebral palsy Genetic disorders- Down Syndrome
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When to consider PAP therapy Confirmed moderate to severe OSA Surgery is not an option Morbid obesity Post-operative T&A with residual OSA Poor surgical candidate Craniofacial syndromes Comoribidities such as ADHD and ESS To stabilize patient prior to surgery In children with milder OSA?
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PAP compliance in children Wide age range Symptoms improve Safe effective treatment Labor intensive >20% drop out Only 50% with immediate acceptance Delayed acceptance in 1 year- 80% in 3 months School age >teens >toddlers Full face harder to accept Compliance varies greatly objective measures important Monitor craniofacial growth
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CPAP and BIPAP for Children Best practices require Child/family focused therapy Health management team approach Coordination of care through RN/RT, sleep lab, DME, and physicians
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MASKS AND MACHINES
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… AND to all a good night.
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References 1.Baldassari C, Kepchar J, et al. Changes in Central Apnea Index following Pediatric Adenotonsillectomy. Otolaryngol Head and Neck Surgery 2012; 146(3) 487–490. 2.Bhattacharjee R, Kheirandish-Gozal L, Spruyt K, et al. Adenotonsillectomy outcomes in treatment of obstructive sleep apnea in children: a multicenter retrospective study. Am J Resp Crit Care Med 2010; 182:676–683. 3.Darrow DH. Surgery for Pediatric Sleep Apnea. Otolaryngol Clin N Am 2007; 40: 855–875. 4.Kerschner J,Lynch JB, et al. Uvulopalatopharyngoplasty with tonsillectomy and adenoidectomy as a treatment for obstructive sleep apnea in neurologically impaied children. International Journal of Pediatric Otorhinolaryngology 2002; 62: 229–235. 5.Lin AC, Koltai PJ. Persistent pediatric obstructive sleep apnea and lingual tonsillectomy. Otolaryngol Head Neck Surg 2009; 141:81–85. 6.Mitchell RB. Adenotonsillectomy for obstructive sleep apnea in children:outcome evaluated by pre and postoperative polysomnography. Laryngoscope 2007; 117:1844–1854. 7.O’Brien LM, Sitha S, Baur LA, Waters KA. Obesity increases the risk for persisting obstructive sleep apnea after treatment in children. Int J Pediatr Otorhinolaryngol 2006; 70:1555–1560. 8.Richter G.T., Rutter M.J, et al. Late-onset laryngomalacia: a variant of disease, Arch. Otolaryngol. Head Neck Surg 2008; 134(1) (2008) 75–80. 9.Shott SR. Evaluation and management of pediatric obstructive sleep apnea beyond tonsillectomy and adenoidectomy. Current Opinion in Otolaryngology & Head and Neck Surgery 2011; 19:449–454. 10.Tauman R, Gulliver TE, Krishna J, et al. Persistence of obstructive sleep apnea syndrome in children after adenotonsillectomy. J Pediatr 2006; 149:803–808. 11.Wooten CT, Shott SR. Evolving therapies to treat retroglossal and base-of tongue obstruction in pediatric obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 2010; 136:983–987.
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Thank You! kwshelly@texaschildrens.org