Neonatal Apnea

Basics

Description

  • Apnea of infancy is an unexplained episode of cessation of breathing for 20 seconds or longer or a shorter respiratory pause associated with bradycardia, cyanosis, pallor, and/or marked hypotonia in infants with gestational age (GA) of 37 weeks or more at the onset of apnea.
  • Apnea of prematurity (AOP) is a pause of breathing for >15–20 seconds or accompanied by oxygen desaturation (Spo2 ≤80% for ≥4 seconds) and bradycardia (heart rate <2/3 of baseline for ≥4 seconds) in infants born <37 weeks GA.
  • Mechanisms of apnea
    • Central apnea
      • Caused by decreased central nervous system (CNS) stimuli to respiratory muscles
      • No evidence of obstruction to airflow but absent chest wall motion
    • Obstructive apnea
      • Can be due to factors such as pharyngeal instability, neck flexion, nasopharyngeal occlusion
      • Characterized by absent airflow but persistent chest wall motion
    • Mixed apnea
      • Mixed etiology, with obstructive apnea preceding (usually) or following central apnea
  • Periodic breathing is a normal neonatal breathing pattern, defined by ≥3 pauses, each ≥3 seconds, with <20 seconds of regular respiration between pauses.

Epidemiology

  • Apnea and bradycardia occur in ~2% of all healthy term infants.
  • AOP is inversely correlated to GA. It occurs in <10% of neonates 34–35 weeks GA and in almost all neonates <28 weeks GA at birth.

Risk Factors

  • Prematurity is the most common cause of apnea.
  • Risk factors common to both AOP and apnea of infancy are as follows:
    • Age (infant <30 days old at higher risk)
    • Upper respiratory tract infections
    • Gastroesophageal reflux (GER)
    • Anemia
    • Cardiac arrhythmias
    • CNS insult (hemorrhage, seizure, tumors)
    • Immunizations (after DTaP injection)
    • Maternal medications, such as magnesium sulfate, prostaglandins, or narcotics

Pathophysiology

  • Immature respiratory control in neonates
    • Immature chemoreceptors in brainstem and in the periphery (carotid body) may lead to decrease in respiratory drive and apnea.
  • Hypoxic ventilatory depression
    • Newborn infants have enhanced sensitivity of respiratory control system to inhibitory neurotransmitters (such as gamma aminobutyric acid [GABA], adenosine, serotonin, and prostaglandin) that can lead to apnea.
  • Impaired hypercapnic ventilatory response
    • Prolonging expiratory time (but not increasing frequency or overall tidal volume) may lead to less minute volume as well as uncoordinated movements of respiratory muscles in response to hypercapnia, resulting in apnea.
  • Laryngeal chemoreflex
    • Activation of laryngeal chemoreceptors (via superior laryngeal nerve afferents) as seen in GER can result in apnea, bradycardia, and hypotension.
  • Sleep state
    • Neonates spend majority of their time in active sleep. Apneas are more common during active sleep when respirations are irregular.
    • Changes in neuromodulatory inputs and generalized inhibition of skeletal muscle activity during sleep are also contributory.
  • Congenital central hypoventilation syndrome (CCHS)
    • Alveolar hypoventilation due to abnormality in the central integration of chemoreceptor information as a result of PHOX2B mutation

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