School's Out for the Summer: Let's learn about Pediatric OSA.
- ZZZPack
- Jul 11, 2019
- 4 min read
Updated: Jul 11, 2019
Today feels like a good day to pay homage to the future of our society-- the children! Yes, kids can also have OSA, and oftentimes the presentation is more subtle, and the management strategy is also different. Kids can have OSA for a variety of reasons, and therefore, they also have a variety of treatment options.
We will focus on what the ICSD-3 has to say about Pediatric OSA in this post.
Definitely expect a lot more coming up about Pediatric OSA as it relates to different co-morbidities, and also treatment modalities.
Let's jump straight in. What are the Diagnostic Criteria?
Criteria A and B must be met.
A. The presence of one or more of the following:
1. Snoring
2. Labored, paradoxical, or obstructed breathing during the child's sleep.
3. Sleepiness, hyperactivity, behavioral problems, or learning problems.
B. PSG demonstrates one or both of the following:
1. One or more obstructive apneas, mixed apneas, or hypopneas, per hour of sleep. (i.e. AHI>1)
OR
2. A pattern of obstructive hypoventilation, defined as at least 25% of total sleep time with hypercapneia (PaCO2 >50 mmHg) in association with one or more of the following:
a. Snoring
b. Flattening of the inspiratory nasal pressure waveform.
c. Paradoxical thoracoabdominal motion.
***So basically: you need an AHI of >1 + obstructive symptoms or behavioral symptoms OR hypoventilaion + obstructive features. This is different than the adult criteria!!
Who do pediatric OSA criteria apply to?
Kids <18 years old.
Note: For scoring purposes, you can use the AASM scoring adult diagnostic criteria for kids aged 13-18 years old.
Other than what is in the diagnostic criteria, what are some other features of OSA in kids?
Upper airway resistance with snoring, but no identifiable flow limitation on PSG. There are negative esophageal pressure swings, and a pattern of cyclic arousals on EEG.
Obstructive events are REM predominant in children.
Kids often do not have cortical arousals on EEG in response to upper airway obstruction, but may have movement or autonomic arousals.
--> why? maybe due to higher arousal threshold
Also, short obstructive apneas can be associated with severe hypoxemia as children have a lower functional residual capacity, and higher metabolic rate than adults.
Note that infants and children with neuromuscular weakness may not snore!
Paradoxical breathing in children with OSA is very prominent due to their compliant rib cages.
Other unique features are strange sleep positions: e.g. extension of the neck.
Prominent sinus arrhythmia.
Secondary enuresis.
Symptoms related to tonsilar hypertrophy: e.g. mouth breathing, frequent URIs, dysphagia.
Up until what age is paradoxical breathing in REM sleep normal?
3 years old.
When is excessive daytime sleepiness a more common feature?
Older children and adolescents, but still less common a symptom than in adults.
What are the Clinical and Pathophysiological Subtypes?
OSA
Obstructive Hypoventilation
Recurrent Arousal Associated with Increased Respiratory Effort (RERA)
What are the demographics of children getting OSA?
Prevalence 1-4%...but getting higher due to obesity epidemic.
Prevalence in Infants and Adolescents not clearly known. Especially in infants this is a controversial subject.
M=F in pre-pubertal children.
M>F in adolescents.
Higher prevalence in black children vs. white children.
Most common in pre-school age (due to adenotonsillar hypertrophy), and then again in adolescence (due to obesity).
What are predisposing and precipitating factors?
What's number 1?
Adenotonsillar hypertrophy and obesity!
Kids with craniofacial abnormalities, e.g. micrognathia, and midface hypoplasia are at risk.
Down Syndrome.
Neuromuscular disease-- accessory muscle weakness, but also upper airway muscle weakness.
Cerebral Palsy, due to spasticity, weakness, incoordination of the upper airway muscles.
GERD: causes upper airway edema, laryngospasm.
Other conditions: mucopolysaccharidosis, sickle cell disease.
Post-op changes: pharyngeal flap operation (usually in children with cleft palate).
Tobacco exposure.
The Apple Doesn't Fall Far from the Tree...
Increased prevalence in children who have a first degree relative with OSA-- relative roles of genetic vs environmental factors have not yet been determined.
Onset, Course, and Complications
Exact course not as well studies as in adults.
Symptoms usually begin within the first few years of life.
Some kids may have improvement of mild OSA with time.
Growth failure, especially when associated with a comorbid genetic or craniofacial symptom can occur. Not good news. Treat that OSA.
Cognitive and behavioral complications are common.
Seizure exacerbation, pulmonary and systemic HTN, and cor pulmonale are also sequelae of untreated OSA.
Pathology and Pathophysiology
Combination of abnormal neuromuscular control and anatomic narrowing of the collapsible part of the upper airway causes OSA.
1. Decreased tone in upper airway muscles during sleep
2. Decrease in ventilatory drive and neuromuscular tone
3. Hypoxemia, hypercapnia and sleep disruption lead to the sequela of OSA, including metabolic and inflammatory anomalies.
4. Adenotonsillar hypertrophy is the main cause of obstruction in normally developing children. Consider other craniofacial abnormalities.
5. Obesity.
What are the Objective Findings of OSA?
Obstructive apneas/hypopneas lasting two breaths in duration-- leads to an EEG arousal or oxygen desaturation of 3%.
***unlike in adults, EEG arousals are not always present after an apnea, but you may see autonomic arousal or muscle arousal.
Upper airway evaluation (e.g. with DISE) can show multiple sites of obstruction. (e.g. tonsils, adenoidal tissue, velum, oropharynx, tongue base, epiglottis)
What is the differential diagnosis?
We're almost at the end!
Isolated Snoring: Children with only snoring can be observed and do not need a PSG. If they have symptoms, then get a PSG. Remember, Home Sleep Apnea tests are not approved for kids.
Central Sleep Apnea: Differentiate via PSG.
Fixed Upper Airway Obstruction: children will have stridor, and symptoms during wake and sleep.
Non-Obstructive Alveolar Hypoventilation: Can co-exist with OSA. These kids do not typically snore, and do not have paradoxical rib motion with breathing.
Other causes of sleepiness, e.g. Narcolepsy, idiopathic hypersomnia, insufficient sleep.
Sleep related epilepsy can mimic OSA during sleep, and you need a full EEG with the PSG to evaluate for this!
Alright, that's a wrap! You've officially read a summary of the Pediatric OSA section of the ICSD-3.
References:
1. American Academy of Sleep Medicine. International classification of sleep disorders, 3rd ed. Darien, IL: American Academy of Sleep medicine, 2014.
2. Stranger Things Image accessed from: https://www.tasteofhome.com/article/stranger-things-cast-ice-cream-flavors/
3. Pediatric PSG Image accessed from: https://obgynkey.com/polysomnography-and-mslt/
4. Childhood Obesity Image accessed from: https://www.deccanchronicle.com/lifestyle/health-and-wellbeing/180516/eating-past-8-p-m-won-t-make-your-kids-fat.html
5. Number 1 Image accessed from: https://www.istockphoto.com/illustrations/number-one-fan?assettype=image&sort=mostpopular&mediatype=illustration&family=creative&phrase=number%20one%20fan
6. Upper airway image accessed from: Blausen.com staff (2014). "Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2).
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