Pediatric Obstructive Sleep Apnea (OSA)

What is OSA?

It is a disorder in which there is upper airway dysfunction causing complete or partial airway obstruction during sleep, leading to decreased oxygen saturation or arousals from sleep.

The obstruction can be mechanical obstruction, dynamic obstruction, or neuromuscular obstruction. The obstruction can be partial or complete. Apnea: cessation of breathing for 10 seconds or more.

Cycles of Sleep

The sleep cycle has two stages

• REM: Rapid eye movement sleep
• NREM: non-rapid eye movement sleep

The sleep cycle begins with stage 1 NREM sleep. The sleep cycle thus transitions from deeper sleep to lighter sleep in 20–30 minutes and then enters the REM sleep pattern. Sleep progression from stage 1 NREM to REM is counted as one sleep cycle, which is around 60 minutes. The sleep cycle in older children is 90 minutes. In the initial hours of sleep, the child experiences deeper planes of sleep. However, beyond the initial couple of hours, the sleep

becomes shallow as the NREM cycles are getting reduced. In the last few hours of sleep (7th and 8th hours), the NREM cycles are limited to almost stage 1 and stage 2 levels of depth.

The duration of REM increases with each cycle. During REM, the patient will have a loss of muscle tone, rapid eye movement, and a dreamy state.

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What is Sleep Disorder Breathing?

Sleep disorder breathing refers to a clinical spectrum of repetitive episodes of complete or partial obstruction of the airway during sleep.

Primary Snoring (PS)

Snoring without obstructive apnea, without arousals from sleep, or without gas exchange abnormalities.

Obstructive Hypoventilation Syndrome (OHS)

There is a persistent partial obstruction of the airways, and there are gas exchange abnormalities. However, there is no apnea in OHS.

Upper Airway Resistance Syndrome (UARS)

There is an increase in negative intrathoracic pressure, especially during inspiration, resulting in arousal and sleep fragmentation. The reason is because of some partial obstruction of the upper airway leading to negative intrathoracic pressure.

Obstructive Sleep Apnea (OSA)

In OSA, there is prolonged airway partial obstruction, or there can be intermittent complete obstruction. When there is a complete obstruction, there is apnea.

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Upper Airway Resistance Syndrome (UARS)

In UARS, snoring is observed due to upper airway narrowing or floppiness. Clinical history suggests sleep fragmentation. PSG shows there is a negative intrathoracic pressure as there

is resistance for airflow in the upper airway. Because of the air resistance, air will not enter the lungs easily, and there is a vacuum of negative pressure. PSG shows:

1. Increased intrathoracic pressure.

2. Flow limitation of nasal pressure monitoring

3. No gas exchange abnormalities

4. Non-REM asynchronous breathing

5. No gas exchange abnormality

Obstructive Hypoventilation Syndrome (OHS)

There is a prolonged period of partial airway obstruction, and it is more common in children than adults. The clinical history of OHS is similar to OSA. PSG demonstrates

• Asynchronous breathing is observed.
• Absence of discrete events
• Sleep fragmentation
• Abnormal gas exchange is observed.
• It may be present only during REM sleep: hypoxia.

   Hypercarbia PetCO > 53 torr.

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Epidemiology

Most studies have shown that 4% to 11% of parents reported apnea. Parents will inform about the sleeping patterns of children, such as snoring, abrupt awakening, starling, or gasping in a repetitive cycle. The precedence of pediatric OSA ranges from 1% to 4%.

depending on the threshold of AHI to diagnose in most patients. The peak age range is 3 to 6 years when adenotonsillar hypertrophy is observed. Gender distribution: males and females are equally affected before puberty. However, after puberty, males are more than females. Furthermore, the prevalence is higher among African Americans and Asian children.

Prematurity is another important factor. Congenital abnormalities like achondroplasia or craniofacial abnormalities have narrow pharyngeal airways that will predispose them to obstruction.

Pathophysiology

In structural factors, there is obstruction in the upper airways. The obstruction can be the level of the nasopharynx or nasal cavity. It could be because of sinusitis, allergic rhinitis or a tumor.

There could also be adenoids in the nasopharynx, causing nasopharyngeal obstruction.

There can be obstruction in the oral cavity and oropharynx due to bulky tongue, aka macroglossia, secondary to some syndromes such as Down's syndrome.

Obstruction can also occur if the child is obese, the palette is sagging down, or lingual tonsil hypertrophy causes structural or mechanical obstruction to the airways.

Lesions are observed at the level of the nose, nasopharynx, oral cavity, larynx (laryngomalacia), and sometimes hypopharynx.

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Neuromuscular tone

In syndromic children having cerebral palsy or genetic disorder, there is a loss of neuromuscular tone. Here, the muscles become floppy and are easily collapsible. So, when the child sleeps, it causes dynamic obstruction. The obstruction is only during sleep. The degree of obstruction is based on the state of REM or NREM.

Inflammation Markers in Pediatric OSA

When there is obstruction to airways, there is hypoxia, which results in oxidative stress and thus causes release of the inflammatory markers.

The inflammatory markers observed are:

• Children often have elevated levels of highly sensitive C- reactive protein (CRP) produced by interleukin activity in the liver.
• High levels of CRP indicate active inflammatory processes and oxidative stress leading to procoagulant activity, prompting atherosclerosis and atherogenesis.
• Endothelin 1 is an inflammatory marker that can be elevated in some patients with OSA, and it is known to decrease postoperatively following adenotonsillectomy.
• Endothelin 1 is a potent vasoconstrictor, and the rise in Endothelin 1 can be associated with cardiovascular risks.

Tumor necrosis factor (TNF) is higher in children with OSA when compared to controls. Myeloid-related protein 8/14, having an important role in the formation of atherosclerosis, has been found to have higher levels in children with OSA, and the levels are in proportion to the severity of the OSA. Children with inflammatory markers over time are at very high risk of cardiac and neurological issues.

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Risk Factors

Common risk factors

• Adenotonsillar hypertrophy
• Upper airway congestion; allergies
• Upper airway obstruction, choanal stenosis, laryngomalacia, subglottic stenosis.
• GER/ LPR
• Cleft palate
• Craniofacial dysmorphism
  • Midfacial hypoplasia - Down's syndrome
  • Micrognathia - Pierre-Robin syndrome
  • Cranial base malformation Achondroplasia

Other risk factors

• Neuromuscular disorder
  • Hypotonia: Down Syndrome muscular dystrophy
  • Spasticity: Cerebral palsy
• Overweight
• Sickle cell disease
• Cystic fibrosis
• Chronic lung disease/BPD
• Scoliosis
• Brain and spinal disorder - Spina Bifida, ACM type II

Also read: Neonatal Respiratory Monitoring

Watch a related video on Management of "Obstructive Sleep Apnea" by Dr. Vyshnavi :

Reducing muscle tone

• Trisomy 21
• Small midface and cranium
• Relative 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 45% to 100%.
• Neuromuscular disease
• Hypothyroidism
• Cerebral palsy
• Moebius, MG
• Reduced central ventilation drive.
  • ACM type I/II
  • Myelomeningocele
  • Brain injury or masses

Medical Conditions

Syndromic children, because of upper airway narrowing in the nasopharynx and oropharynx, can have sleep apnea. Syndromes includes

• Craniofacial syndromes
• Apert
• Crouzon
• Pierre-robin
• Treacher-Collins
• Pfeiffer
• Achondroplasia
• Beckwith-Wiedemann
• Goldenhar syndrome
• Marfan
• Prader Willi
• Sickle cell disease
• Prematurity/ CLD

Also read: Neonatal Cholestasis: Causes, Diagnosis, and Treatment in Infants

How to Manage OSA?

Intervention is absolutely necessary in any child with AHI > 5. While there is less consensus regarding the AHI between 1 and 5. Choice of treatments involves surgeries like:

• Adenotonsillectomy: First line of therapy
• Turbinate reduction
• Craniofacial therapy
  • Mandibular advancement
  • Lefort osteotomies and maxillary distraction
• Uvulopalatopharyngoplasty: not recommended
• Tracheostomy

Medical therapies

Weight loss is a necessary measure. CPAP is used if there is failure after Adenotonsillectomy

or tonsillectomy. Children with neuromuscular issues can also opt for CPAP. Intranasal steroids can help patients with allergic rhinitis or sinusitis. Oral appliances can also assist. Positional therapy and snore aids are other medical therapies.

Adenotonsillectomy

It is the first line of treatment, a gold standard. The presence of risk factors is not a contraindication to adenotonsillectomy. The residual OSA is observed in almost 25% of patients.

Therefore, reassessment of the high-risk group should be done post-surgery, and PSG is recommended. High-risk patients for postoperative respiratory complications in children with OSAS undergoing adenotonsillectomy are:

• Children younger than 3 years
• Someone having severe OSAS on PSG, AHI>10
• Patients with pulmonary hypertension, congenital heart disease, prematurity, CLD, recent URI, morbid obesity, trisomy 21, craniofacial abnormalities, neuromuscular disorders, CP, and asthma.

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Severe OSA

Patients have shown significant improvement in the RDI and quality of life of the children with severe OSA. OSA does not resolve completely. However, postoperative PSG is necessary for any additional therapy. Jaw distraction (bidirectional distraction osteoneogenesis)

has proven to be a reliable technique in producing an adequate pharyngeal airway in children with micrognathia and subsequent pharyngeal restriction secondary to tongue base collapse.

Rapid maxillary expansion has also been proposed as an alternative technique in children with retrognathia. Tongue-based reduction can help syndromic children with macroglossia, Beckwith-Wiedemann, or Down syndrome. Post-OP complications

• Bleeding
• Increased risk of perioperative respiratory complications.
• They may be more sensitive to opiates and inhalational anaesthetic agents and are at risk of pulmonary oedema.
• In children who have been identified as high-risk, surgery should be performed in a hospital with pediatric intensive care facilities.
• In cases at high risk of airway compromise, a nasopharyngeal airway can help reduce the reliance on PICU.

Points to Remember

• Pediatric OSA is a common condition but also often missed.
• Understanding pathophysiology is crucial, along with an appreciation for the history and examination of the diagnosis.
• Conditions need to be careful and relative to the predictive values.
• Interventions can help in a good sustainable development in the quality of life. However, good awareness of the comorbidities is essential for better outcomes.

Hope you found this blog helpful for your NEET SS Pediatrics ENT Preparation. For more informative and interesting posts like these, keep reading PrepLadder’s blogs.

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