Sleep Apnea—Obstructive Sleep Apnea Syndrome

Sleep Apnea—Obstructive Sleep Apnea Syndrome: Excerpt from The 5-Minute Pediatric Consult

Akinyemi O. Ajayi, MD

Sleep Apnea—Obstructive Sleep Apnea Syndrome - BASICS

Sleep Apnea—Obstructive Sleep Apnea Syndrome - description

• Sleep-disordered breathing encompasses a range of breathing disorders occurring during sleep. These conditions include primary snoring (PS), respiratory events related to arousals (RERA), and obstructive sleep apnea syndrome (OSAS).
• Obstructive apnea is defined as the cessation of air flow at the nose and mouth despite respiratory effort, associated with some gas-exchange abnormality and/or loss of regular sleep patterns.
• Distinct from central apnea (cessation of air flow that is not accompanied by respiratory effort), which indicates brain immaturity or dysfunction
• Many children with OSAS exhibit partial airway obstruction. This is known as obstructive hypoventilation or hypopnea and is more commonly seen in children than is complete obstruction.
• OSAS may be subdivided into mild, moderate, and severe forms according to degree of severity.
• Upper airway resistance syndrome is a respiratory disorder characterized by partial airway obstruction and arousals leading to sleep fragmentation, and is not associated with gas-exchange abnormalities.
• PS or habitual snoring implies snoring that does not lead to abnormalities in gas exchange or sleep fragmentation.
• Central apnea up to 20 seconds may be a normal finding in premature or newborn infants during the first months of life.
• Periodic breathing: Three or more episodes of central apnea lasting at least 3 seconds each, separated by <20 seconds. Periodic breathing may be found in the newborn; however, it should not exceed >4% of sleep time (from a sleep study) and is not associated with bradycardia or hypoxemia.

• Habitual snoring may be confused with snoring causing clinical upper airway obstruction. The need for polysomnography depends on the patient’s symptoms.
• Normal-size tonsils do not exclude OSAS.
• Tonsillar size does not predict the presence of OSAS.
• Treatment of gastroesophageal reflux in infants with obstructive apnea may be helpful even in the absence of obvious symptoms of reflux.

Sleep Apnea—Obstructive Sleep Apnea Syndrome - epidemiology

Sleep Apnea—Obstructive Sleep Apnea Syndrome - incidence

Pediatric incidence estimated to be between 1% and 2% for OSAS, whereas the incidence of PS is between 8% and 10%. In obesity, the incidence is as high as 30% in children.

Sleep Apnea—Obstructive Sleep Apnea Syndrome - risk factors

Sleep Apnea—Obstructive Sleep Apnea Syndrome - genetics

• In prepubertal children, OSAS occurs equally in boys and girls. However, in adults, OSAS is more common in men.
• Any condition that affects either the airway tone or structure can increase the risk of OSAS.
• Several genetic disorders with associated craniofacial anomalies, hypotonia, and obesity may lead to OSAS. These include:
  • Pierre Robin syndrome
  • Treacher Collins syndrome
  • Down syndrome
  • Mucopolysaccharide disorders
  • Arnold–Chiari malformations
  • Prader–Willi syndrome
  • Hereditary neuromuscular disorders

Sleep Apnea—Obstructive Sleep Apnea Syndrome - pathophysiology

• The peak incidence of OSAS in children is between 2 and 6 years of age, most commonly associated with adenotonsillar hypertrophy in combination with neuromuscular factors.
• In infants, OSAS is uncommon; however, it may exist with craniofacial anomalies, neurologic disorders associated with low muscle tone, laryngomalacia or tracheomalacia, and gastroesophageal reflux.
• Impaired arousal mechanisms also contribute to abnormalities seen in OSAS.
• In older children, OSAS may be associated with obesity. This form may resemble the adult type of OSAS.

Sleep Apnea—Obstructive Sleep Apnea Syndrome - associated conditions

• Adenotonsillar hypertrophy
• Craniofacial anomalies including midfacial hypoplasia and mandibular hypoplasia.
• Laryngomalacia
• Neurologic and neuromuscular disorders that cause hypotonia may underlie poor ventilation during sleep.
• Gastroesophageal reflux
• Obesity
• Metabolic disorders
• Allergic rhinitis, nasal septum deviation, nasal polyps
• Sedatives, seizure medications, and anesthesia

Sleep Apnea—Obstructive Sleep Apnea Syndrome - DIAGNOSIS

Sleep Apnea—Obstructive Sleep Apnea Syndrome - signs & symptoms

Sleep Apnea—Obstructive Sleep Apnea Syndrome - history

• Nocturnal symptoms include difficulty breathing when asleep, snoring, apnea, and restless sleep with frequent arousals.
• Daytime symptoms: Excessive sleepiness, frequent upper respiratory/ear infections, conductive hearing loss, mouth breathing, poor appetite, and a hyponasal voice
• Other concerns: ADHD, gastroesophageal reflux, poor school performance, and headaches (especially in the morning and upon awakening)
  • OSAS rarely produces these symptoms acutely, but tends to occur over weeks to months.
  • Parents may notice that symptoms worsen with upper respiratory infections.
• The possibility of sleep-disordered breathing or a primary sleep disorder should be considered in children evaluated for attention deficit hyperactivity disorder.

Sleep Apnea—Obstructive Sleep Apnea Syndrome - physical exam

• Assessment of the child’s growth. In severe cases of OSAS, failure to thrive has been reported.
• Obesity remains a risk factor, especially in older children.
• Assessment of tonsillar size
• Presence of mouth breathing, hyponasal speech, adenoidal facies, midfacial hypoplasia, retrognathia, micrognathia, or other craniofacial anomalies may be present at times and may suggest the diagnosis.
• Nasal obstruction due to polyps, nasal septum deviation, turbinate hypertrophy, or congestion
• Tongue size
• Mobility and elevation of the soft palate; hard palate integrity
• In extreme cases, cardiac involvement may lead to cor pulmonale and heart failure. Examination may suggest signs of pulmonary hypertension or congestive heart failure, such as an increased second heart sound.
• A neurologic examination to evaluate general muscle strength, tone, and developmental status, especially in infants and children who do not improve after adenotonsillectomy

Sleep Apnea—Obstructive Sleep Apnea Syndrome - tests

Sleep Apnea—Obstructive Sleep Apnea Syndrome - lab

• Polysomnography:
  • The gold standard for the diagnosis of OSAS is nocturnal polysomnography, to differentiate the type of sleep apnea and to assess severity.
  • Polysomnography is an 8–10-hour-long multichannel study performed in a controlled setting that can assess respiratory and/or sleep abnormalities.
  • Indices such as oxygenation, ventilation, apnea index (AI), apnea hypopnea index (AHI), arousal index, arousal awakening index, and periodic limb movements index are determined along with sleep parameters such as sleep efficiency and sleep stages.
  • Monitoring includes EEG, electro-oculogram, electromyogram, arterial oxygen saturation, end tidal CONormative respiratory and sleep variables for children have recently been published and include an apnea-hypopnea index of <1 being normal.
  • Scoring for pediatric polysomnography differs from that of adults. This includes using 2 respiratory cycles to define both obstructive apnea and central apnea or 2 respiratory cycles associated with a 30% decline in airflow and a >4% decline in oxygen level to define hypopnea. Lower AHI values are considered significant in children, compared to adults.
• Other studies:
  • Validated questionnaires are helpful to screen for OSAS in the office.
  • Routine blood work is generally noncontributory; in severe forms, polycythemia, hypercarbia, and elevated bicarbonate may be noted.
  • Evaluation for gastroesophageal reflux may include pH monitoring during sleep, barium swallow, or radionuclide studies (milk scan).

Sleep Apnea—Obstructive Sleep Apnea Syndrome - imaging

• Lateral neck x-ray is easy to perform to assess adenoid and tonsillar size, as well as patency of the nasopharyngeal airway.
• Nocturnal audio- and videotaping, as well as abbreviated nap polysomnography, are useful studies if the results are positive, but generally have a poor negative predictive value.
• Upper airway endoscopy as well as bronchoscopy may be performed to evaluate anatomic or dynamic causes for airway obstruction (pharyngeal hypotonia, pharyngeal stenosis, laryngotracheomalacia, vocal cord polyps, papilloma).
• Head or neck CT or MRI should be considered for complex craniofacial anomalies. If central apnea is noted, then MRI studies should also evaluate the brain stem to evaluate for an Arnold–Chiari malformation.
• In severe cases of OSAS, a cardiac evaluation, including ECG, chest x-ray, and Doppler ECG, may be indicated.

Sleep Apnea—Obstructive Sleep Apnea Syndrome - differencial diagnosis

• PS or habitual snoring: By definition is not associated with sleep-disordered breathing, but may progress to OSAS. Between 20% and 50% of children with habitual snoring may have OSAS.
• Upper airway resistance syndrome: This condition is associated with sleep fragmentation and daytime sleepiness.
• Obesity–hypoventilation syndrome: A variant of OSAS
• Central apnea and periodic breathing
• Congenital central hypoventilation syndrome
• Other causes of excessive daytime sleepiness include:
  • Disorganized home environment, emotional stress
  • Substance abuse/drug intoxication: Psychotropic medications, antihistamines, anticonvulsants, narcotics
  • Narcolepsy: Onset typically around adolescence, but cataplexy may occur later and delay the diagnosis.
    • Classic tetrad of symptoms of narcolepsy includes excessive daytime somnolence, cataplexy, hypnagogic hallucinations, and sleep paralysis.
    • In addition, fragmented night time sleep may be seen.
  • Epilepsy: Absence spells of unresponsiveness, electroencephalogram changes
• Causes of obstructive apnea include any cause of lymphoidal hypertrophy in the upper airway (allergies viral/bacterial tonsillitis, neoplasm, epiglottitis, retropharyngeal abscess); chronic phenytoin exposure; and excessive storage material in upper airway submucosa.
• Causes of abnormal laxity of upper airway soft tissues: Down syndrome, acute polyneuropathy (Guillain–Barré syndrome), chronic neuromuscular disease, Prader–Willi syndrome, myasthenia gravis
• Causes of abnormal control/coordination of upper airway musculature: Almost any cause of diffuse CNS dysfunction, including cerebral palsy, and acquired lesions of the CNS such as stroke and head trauma.
• Causes of central apnea: Beyond infancy, most commonly due to drugs that suppress ventilatory drive; in premature infants may be due to nonspecific immaturity of neural ventilatory control mechanism, sepsis, and, rarely, seizures, brainstem compression, brain tumors, Arnold–Chiari type 2 (although increasingly seen with type 1)
• Reflux may potentiate central apnea and should be investigated (see “Gastroesophageal Reflux” topic).
• Androgen steroids may cause central apnea in adults.

Sleep Apnea—Obstructive Sleep Apnea Syndrome - TREATMENT

Sleep Apnea—Obstructive Sleep Apnea Syndrome - initial stabilization

• OSAS is usually an insidious disorder.
• Mild and moderate cases may be treated on an elective or urgent basis. However, severe cases may require urgent intervention.
• Severe cases of upper airway obstruction are usually diagnosed during polysomnography or during procedures involving sedation or anesthesia.
  • Ensure adequate ventilation and oxygenation, with quick assessment of the cause.
  • Temporary relief of the obstruction should be undertaken by an experienced team.
  • Transfer to an intensive care unit where the airway can be monitored carefully.
  • Following relief of airway obstruction, pulmonary and airway edema, as well as copious secretion production, may develop.
  • Modalities of care should include: Placement of a nasopharyngeal airway, noninvasive ventilation with continuous positive airway pressure/bilevel positive airway pressure (CPAP/BiPAP), or placement of an endotracheal tube for mechanical ventilation
• Risk factors for postoperative complications in children with OSAS include age <3 years, severe OSAS, pulmonary hypertension, obesity, prematurity, failure to thrive, craniofacial or neuromuscular disorders, and/or upper respiratory tract infection.

Sleep Apnea—Obstructive Sleep Apnea Syndrome - general measures

• In most cases, adenotonsillectomy is first-line therapy. However, some patients continue to have significant postoperative OSAS that requires further evaluation.
• Noninvasive ventilatory support with CPAP or BiPAP may be helpful.
• In complicated cases, when craniofacial malformations are involved, surgical procedures such as tongue reduction, uvulopalatopharyngoplasty, or mandibular or maxillary advancement may be indicated.
• When there is evidence of gastroesophageal reflux, treatment with acid-suppression agents and chalasia precautions are indicated.
• Weight loss may be useful in obese children.
• Laser surgery and dental appliances may be useful in adults with mild OSAS, but there is no experience with these approaches in children.
• In extreme cases, a tracheostomy may be indicated, especially when significant craniofacial abnormalities exist.

Sleep Apnea—Obstructive Sleep Apnea Syndrome - FOLLOW UP

Sleep Apnea—Obstructive Sleep Apnea Syndrome - complications

Complications are due to chronic hypoxemia, hypercarbia, acidosis, as well as impaired sleep and include:

• Pulmonary hypertension, later cor pulmonale (rare)
• Systemic hypertension has been reported in adults and a few pediatric cases.
• Congestive heart failure; arrhythmias are common in adults with underlying coronary artery disease.
• Neurodevelopmental complications: Daytime somnolence, poor school performance, hyperactivity, and social withdrawal
• Poor growth and failure to thrive
• Postanesthesia respiratory failure and death have been reported in children with OSAS.

Sleep Apnea—Obstructive Sleep Apnea Syndrome - patient monitoring

• Clinical improvement is expected soon after adenotonsillectomy. In children <1 year of age with severe forms of OSAS, underlying craniofacial anomalies, or neurologic disorders, repeat overnight polysomnography is indicated 6–8 weeks after surgery.
• Regrowth of adenoid tissue may occur months to years after adenoidectomy. Therefore, if clinical symptoms, such as snoring, difficulty breathing while asleep, or a decline in school performance recur, a re-evaluation is indicated.
• Follow-up sleep studies may help to monitor therapy.

Sleep Apnea—Obstructive Sleep Apnea Syndrome - bibliography

International Classification of Sleep Disorders, 2nd ed. American Academy of Sleep Medicine; 2005:56–60.American Sleep Apnea Association. Available at http://www.sleepapnea.org.
1. D’Andrea LA. Diagnostic studies in the assessment of pediatric sleep-disordered breathing: Techniques and indications. Pediatr Clin North Am. 2004;51(1):169–186.
2. Farber JM. Clinical practice guidelines: Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2002;109(4):704–712.
3. Marcus CL. Sleep-disordered breathing in children. Am J Respir Crit Care Med. 2001;164:16–30.
4. O’Brien LM. Neurobehavioral implications of habitual snoring in Children. Pediatrics. 2004;114:44–49.
5. Rosen CL. Obstructive sleep apnea syndrome in children: Controversies in diagnosis and treatment. Pediatr Clin North Am. 2004;51(1):153–167, vii.

Sleep Apnea—Obstructive Sleep Apnea Syndrome - CODES

Sleep Apnea—Obstructive Sleep Apnea Syndrome - icd9

• 327.20 Organic sleep apnea, unspecified
• 327.23 Obstructive sleep apnea (adult) (pediatric)

Sleep Apnea—Obstructive Sleep Apnea Syndrome - FAQ

• Q: Can my child still have OSAS after adenotonsillectomy?
• A: Yes, at times the adenoid tissue can grow back again. In addition, some cases of OSAS are related to a small upper airway that is restricted by anatomic or neurologic conditions. In these cases, adenotonsillectomy will not always resolve OSAS.
• Q: Does OSAS cause neurologic problems?
• A: Several studies suggest neurocognitive deficits in children with OSAS. The most common findings include reduced school performance and ADHD.

Book Source Details

• Book Title: The 5-Minute Pediatric Consult
• Author(s): M. William Schwartz MD; et al.
• Year of Publication: 2008
• Copyright Details: The 5-Minute Pediatric Consult, Copyright © 2008 Lippincott Williams & Wilkins.

More About Obstructive sleep apnea

• Back to disease: Obstructive sleep apnea: Introduction
• Next Book Extract About Obstructive sleep apnea: Surveys relating to Obstructive sleep apnea
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: The 5-Minute Pediatric Consult Authors: M. William Schwartz MD; et al. Publisher: Lippincott Williams & Wilkins Copyright: 2008 ISBN: 0-7817-7577-9

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