Apnea of Prematurity (NeoReviews 2007;8:e214, NeoReviews 2002;3:e59)
• Cessation of breathing >15 sec usually associated with desats and bradycardia. Characterized as obstructive, central, or mixed
• Occurs in 85% neonates less than 34 wk gestation; can persist up to 42 wk
• Pathophysiology
• Immaturity of the central respiratory drive in response to hypercapnia, hypoxia and exaggerated inhibitory response to stimulation of airway receptors
• Premature infants are predisposed to upper airway obstruction and desats during sleep due to poor airway stability
• Periodic breathing: Benign condition consisting of regular, recurring cycles of breathing of 10–15 sec duration interrupted by pauses of at least 3 sec. More common in
premature infants. Respiratory pauses are self-limited and ventilation continues. No treatment necessary
• Apnea of infancy: Apnea that persists beyond 37 wk gestation
• Diagnosis
• Often evident on continuous cardiorespiratory monitoring. Definitive diagnosis with pneumogram. Rule out infection
• Treatment
• Supplemental O2, nasal CPAP to prevent airway collapse and alveolar atelectasis
• Caffeine (loading dose 20 mg/kg followed by maintenance of 5–10 mg/kg q24h) to stimulate CNS and respiratory muscle function
• Consider treatment of GER
Central Apnea
• Pauses in respiration due to lack of signal from brain to initiate breath. Usually related to abnormality within brainstem or congenital
• Causes
• Congenital central hypoventilation syndrome (CCHS, Ondine’s curse). Associated with Hirschsprung disease, neural crest tumors. Often due to PHOX2B mutation
• Acquired central hypoventilation, such as a stroke or tumor of the brainstem
• May be associated with cerebral palsy, tumors or other structural brainstem abnormality
• Diagnosis
• Polysomnogram: Distinguishes obstruct vs. central apnea
• Treatment: Bipap, tracheostomy and vent. Supplemental oxygen will treat desats with apnea but will not address ventilation
Obstructive Sleep Apnea (Arch Pediatr Adolesc Med 2005;159:775;
Pediatrics 2002;109:704)
• Breathing disorder during sleep w/ prolonged partial upper airway obstruct and/or intermittent complete obstruct (obstructive apnea); disrupts ventilation and sleep
• Needs to be distinguished from 1° snoring, defined as snoring w/o obstructive apnea, frequent arousals from sleep, or gas exchange abnormalities
• Clinical manifestations
• Chronic snoring, daytime fatigue/sleepiness, sleepwalking/-talking, enuresis, periodic limb movement, headaches
• Mouth breathing, nasal obstruct w/ wakefulness, adenoidal facies, hyponasal speech
• Neurocognitive deficits: Poor learning, behavioral problems, ADHD
• Risk factors: Adenotonsillar hypertrophy, obesity, craniofacial anom, neuromuscular d/o
• Diagnosis
• PSG: Can distinguish 1° snoring from OSAS, assess severity and stratify patients likely to have post-tonsillectomy complication, allows titration to optimal level of CPAP
• Treatment
• Weight loss
• Adenotonsillectomy: The most common treatment for children with OSAS. Resolution occurs in 75–100% after adenotonsillectomy
• CPAP: Used indefinitely
• Surgery: Mandibular extraction, hypoglossal nerve stimulation
• Complications
• Neurocognitive impairment, behavioral problems, FTT, cor pulmonale
• Metabolic sequelae (HTN, insulin resistance, dyslipidemia) in obese children
• Caution with sedation, surgery–increased risk of airway compromise. Risk of
post-obstructive pulmonary edema following T&A