Apnea In Children


Article Author:
Noah Kondamudi


Article Editor:
Shailesh Khetarpal


Editors In Chief:
Eric Flake


Managing Editors:
Carrie Smith
Abdul Waheed
Frank Smeeks
Kristina Soman-Faulkner
Scott Dulebohn
Sobhan Daneshfar
William Gossman
Pritesh Sheth
John Shell
Matthew Varacallo
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Richard Ciresi
Hajira Basit
Phillip Hynes


Updated:
3/6/2019 11:41:57 AM

Introduction

Apnea can be defined as cessation of respiratory effort lasting more than 20 seconds, or if shorter duration, accompanied with bradycardia or cyanosis. Apneic episodes are more common in infants and premature babies, but they can occur at any age. Although there is considerable overlap between causes of apnea in infants and children, the etiology among older children is similar to that of adults. Apnea can be a manifestation of a variety of serious conditions, and at the outset should be differentiated from benign causes such as breath-holding spells and snoring. Apnea could be central (depressed respiratory center with no efferent output), obstructive (obstruction to airflow causing inadequate ventilation) or mixed (both central and obstructive).[1][2][3][4][5]

Etiology

While the most frequent cause of apnea in infants is idiopathic, obstructive sleep apnea due to tonsil/adenoidal hypertrophy, often coexisting with obesity, is the most common cause in children. Other conditions that predispose individuals to obstructive sleep apnea (OSA) include:

  • Craniofacial anomalies (Pierre Robin sequence, Beckwith-Wiedemann syndrome, Apert syndrome, Treacher Collins syndrome)
  • Chronic nasal obstruction (severe septal deviation, allergic rhinitis, nasal polyps)
  • Down syndrome
  • Metabolic abnormalities (mucopolysaccharidosis)
  • Infections (supraglottis, croup, bronchiolitis, pneumonia)
  • Asthma attacks,
  • Foreign body in the airway 
  • Congenital chest wall deformities.

Sickle cell anemia has been associated with OSA, but its mechanism is unclear. Predominant central causes of apnea include central nervous system (CNS) infections, raised intracranial pressure (accidental or inflicted head trauma, hydrocephalus, tumors), toxin exposures (CNS depressants, carbon monoxide poisoning), and central idiopathic hypoventilation. Neuromuscular disorders (Guillain-Barré syndrome, Duchenne muscular dystrophy, Werdnig-Hoffman disease) often cause mixed apnea. Morbid obesity itself can cause hypoventilation (Pickwickian syndrome) and predispose to apnea. Laryngospasm can occur as a protective reflex during episodes of gastroesophageal reflux and should be suspected when episodes are associated with feeding. [6][7][8][9]

Epidemiology

There are no good epidemiological studies related to apnea in children and very few studies related to OSA. The prevalence of OSA among otherwise healthy children is estimated to be 1% to 3%, and obesity is thought to increase this risk by four to five times. OSA is more common among black (3.5 times higher) and Hispanic children than white children. Most children with obstructive sleep apnea are aged between 2 to 10 years and usually present around four years of age.

Pathophysiology

Central apnea is a result of direct depression of the respiratory center affecting its efferent outputs that stimulate breathing. Neuromuscular disorders cause both central and obstructive apnea (impaired pharyngeal tone and paralysis of the respiratory muscles).

The pathophysiology of obstructive sleep apnea is not as clear. Professionals speculate that airway obstruction triggers electrocortical arousal which activates the autonomic nervous system that stimulates increased respiratory effort and tachypnea. There may also be subtle alterations to the central chemosensitive arousal network, particularly to hypercapnia in addition to diminished laryngeal reflexes to mechanoreceptor and chemoreceptor stimulation. These blunted responses are thought to play a role in obstructive sleep apnea. Furthermore, children develop oxygen desaturation much earlier than adults due to their higher respiratory rates for a similar degree of obstruction. Most children with obstructive sleep apnea have impaired arousal responses to inspiratory stimuli during rapid eye movement (REM) and non-REM sleep. The key element of obstructed sleep apnea is disordered breathing in sleep that manifests as both apnea and hypopnea.

History and Physical

A detailed history characterizing the event in terms of duration and associated symptoms, including a change in color and mental status, relationship to sleep, and feeding should be obtained.  History with a particular focus on prematurity, known congenital, metabolic or genetic disorders, neurological conditions and previous similar episodes should be obtained. Any possibility of exposure to toxic substances should be ascertained. A family history of snoring, exposure to tobacco smoke, and nasal allergies are all strongly associated with obstructive sleep apnea. History of fever, cough, and rhinorrhea suggests an infectious cause and chronic mouth breathing and snoring. Excessive daytime sleeping suggests upper airway obstruction. Other symptoms of OSA include restlessness, frequent nightmares, difficulty to wake up, enuresis, other behavior problems, and overall irregular sleep patterns.

Abnormal vital signs should be addressed emergently, but in most cases, the child appears well at the time of evaluation. Abnormal size and appearance of the child may offer clues towards identifying an underlying metabolic or genetic abnormality, and unexplained skin bruises may suggest child abuse. Cyanosis represents poor perfusion or hypoxia, and pallor is suggestive of anemia.

Altered mental status, bulging fontanelles indicate increased intracranial pressure and presence of fever and rhinorrhea suggests upper airway infection or bronchiolitis. Sonorous breathing indicates obstruction at the pharyngeal level (tonsil/adenoidal hypertrophy), stridor suggests upper airway obstruction and wheeze lower airway obstruction (asthma). Characteristic adenoid facies (underdeveloped thin nostrils, short upper lip, prominent upper teeth, crowded teeth, narrow upper alveolus, high-arched palate, hypoplastic maxilla) with mouth breathing, nasal speech, and periorbital swelling may be present in 15% to 20% of children with OSA.

Evaluation

The performance of lab and imaging studies should be based on indications uncovered by the history and physical examination. If OSA is suspected, polysomnography is considered to be the gold standard for diagnosis and determination of severity. Lateral neck x-rays may show adenoidal hypertrophy or other abnormalities, but these are not diagnostic. Pulse oximetry when asleep and/or sleep questionnaires may be used to identify children when polysomnography is not feasible.[10][11][12][9]

Treatment / Management

The management of apnea in infants is geared toward identifying the underlying cause, and therapeutic interventions are directed toward the identified condition. For OSA, the first-line treatment is adenotonsillectomy, with other options being tonsillotomy, tongue reduction surgeries, and tracheostomy in selected patients. While continuous positive airway pressure (CPAP) is the mainstay of therapy for most adults, though effective for moderate OSA, these devices are hard to use in children as they are not well tolerated.

Overall medical therapy has limited value in OSA. Fluticasone administered nasally for six weeks reduced the frequency of obstructive events in children, but the effect is not long lasting, and it was used in mild OSA. Systemic steroids have no role in treating OSA. In a double-blind, randomized control trial, oral montelukast for six weeks decreased the severity of OSA and adenoidal hypertrophy. Consultation with specialists should be based on the identified cause of apnea.

Pearls and Other Issues

Long-term consequences of untreated OSA include neurocognitive disabilities, behavior problems, growth failure, pectus excavatum, scoliosis, pulmonary hypertension, and cor-pulmonale.

A polysomnographic-derived index known as the apnea-hypopnea index (apnea-hypopnea index equals the total number of apneas and hypopneas/total duration of sleep in hours) can be used to determine severity. An apnea-hypopnea index of less than one is considered to be normal in children. An apnea-hypopnea index of more than 20 is considered severely abnormal.

Enhancing Healthcare Team Outcomes

The diagnosis and management of apnea in children is with a multidisciplinary team that includes the pediatrician, nurse practitioner, primary care provider, neurologist, radiologist, and the sleep specialist. The management of apnea in infants is geared toward identifying the underlying cause, and therapeutic interventions are directed toward the identified condition.

Consultation with specialists should be based on the identified cause of apnea. The outcomes depend on the cause but if apnea is left untreated, it can have serious repercussions on growth, intellect and functioning. [13][14]


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Apnea In Children - Questions

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A well appearing, 3 month old afebrile infant is brought to the ED by his parents. The mother states that the child turned blue for a few seconds. Which one of the following is not a likely diagnosis?



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A 4-month-old female is brought to the emergency room after she stops breathing for about 30 seconds. The mother reports her lips became blue and she didn't resume breathing until she blew in her face. The patient had no symptoms before the event. She is breastfed and has had all recommended immunizations. The mother's first child died of SIDS. On exam, the patient is irritable and alert. There is dried blood at both nares. Oxygen saturation is 97 percent on room air. The rest of the exam is normal. What is indicated by the physical exam and the fact that the first child died from SIDS?



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What is the gold standard to diagnose obstructive sleep apnea in children?



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Which of the following is not a long-term consequence of obstructive sleep apnea in children?



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In patients with chronic obstructive sleep apnea, which of the following treatment modalities are not recommended?



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Apnea In Children - References

References

Proenca-Modena JL,de Souza Cardoso R,Criado MF,Milanez GP,de Souza WM,Parise PL,Bertol JW,de Jesus BLS,Prates MCM,Silva ML,Buzatto GP,Demarco RC,Valera FCP,Tamashiro E,Anselmo-Lima WT,Arruda E, Human adenovirus replication and persistence in hypertrophic adenoids and palatine tonsils in children. Journal of medical virology. 2019 Feb 28;     [PubMed]
Ahmad N,Bawazir OA, Assessment and preparation of obese adolescents for bariatric surgery. International journal of pediatrics     [PubMed]
Armoni Domany K,He Z,Nava-Guerra L,Khoo MCK,Xu Y,Hossain MM,DiFrancesco M,McConnell K,Amin R, The Effect of Adenotonsillectomy on Ventilatory Control in Children with Obstructive Sleep Apnea. Sleep. 2019 Feb 26;     [PubMed]
Silverio A,Khalili SP,Cunningham A, An exploratory look at comorbidities, utilization, and quality of care among obese and nonobese children in academic family medicine practice. International journal of pediatrics     [PubMed]
Adamson R,Palen B,He K,Wrede J,O'Hearn D,Parsons E, Introduction to Obstructive Sleep Apnea for the Internist. MedEdPORTAL : the journal of teaching and learning resources. 2018 Oct 9;     [PubMed]
Mitchell RB,Archer SM,Ishman SL,Rosenfeld RM,Coles S,Finestone SA,Friedman NR,Giordano T,Hildrew DM,Kim TW,Lloyd RM,Parikh SR,Shulman ST,Walner DL,Walsh SA,Nnacheta LC, Clinical Practice Guideline: Tonsillectomy in Children (Update). Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery. 2019 Feb;     [PubMed]
Hilmisson H,Lange N,Magnusdottir S, Objective sleep quality and metabolic risk in healthy weight children results from the randomized Childhood Adenotonsillectomy Trial (CHAT). Sleep     [PubMed]
Chen J,He S, Drug-induced sleep endoscopy-directed adenotonsillectomy in pediatric obstructive sleep apnea with small tonsils. PloS one. 2019;     [PubMed]
Graef DM,Byars KC, Utility of the Sleep Disorders Inventory for Students in Clinically Referred Youth With Insomnia: Risk Identification and Relationship With Polysomnographic Measures. Behavioral sleep medicine. 2019 Feb 22;     [PubMed]
Smith DF,Amin RS, Obstructive Sleep Apnea and Cardiovascular Risk in Pediatrics. Chest. 2019 Feb 18;     [PubMed]
Scheffler P,Wolter NE,Narang I,Amin R,Holler T,Ishman SL,Propst EJ, Surgery for Obstructive Sleep Apnea in Obese Children: Literature Review and Meta-analysis. Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery. 2019 Feb 19;     [PubMed]
Akkina SR,Ma CC,Kirkham EM,Horn DL,Chen ML,Parikh SR, Does drug induced sleep endoscopy-directed surgery improve polysomnography measures in children with Down Syndrome and obstructive sleep apnea? Acta oto-laryngologica. 2018 Nov;     [PubMed]
Kohn JL,Patel P,Levi JR,Cohen MB, Outcomes of Children with Mild Obstructive Sleep Apnea Treated Nonsurgically: A Retrospective Review. Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery. 2019 Feb 12;     [PubMed]
Bergeron M,Duggins A,Chini B,Ishman SL, Clinical outcomes after shared decision-making tools with families of children with obstructive sleep apnea without tonsillar hypertrophy. The Laryngoscope. 2019 Jan 7;     [PubMed]

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