Neonatal Apnea

Descriptive text is not available for this imageBASICS

DESCRIPTION

  • Apnea of infancy
    • Any cessation in breathing for >15 to 20 seconds or cessation in breathing <15 seconds if accompanied by oxygen desaturation and bradycardia, cyanosis, pallor, and/or marked hypotonia in infants with gestational age (GA) of ≥37 weeks at the onset of apnea.
  • Apnea of prematurity (AOP)
    • Apnea lasting at least 15 to 20 seconds or shorter duration apnea if accompanied by bradycardia and/or hypoxia, in an infant born at <37 weeks GA
    • Apnea is the best-known indicator of immature control of breathing.
  • Periodic breathing
    • A normal neonatal breathing pattern, defined by ≥3 pauses, each ≥3 seconds, with <20 seconds of regular respiration between pauses.
    • Not generally sufficient to cause bradycardia or desaturation
  • Classification of apnea based on respiratory effort and airflow
    • Central apnea
      • Cessation of respiratory effort without evidence of obstruction to airflow
      • Absence of chest wall motion
      • Caused by decreased central nervous system (CNS) stimuli to respiratory muscles
    • Obstructive apnea
      • Cessation of airflow despite respiratory effort
      • Persistent chest wall motion
      • Often caused by pharyngeal instability, neck flexion, or nasopharyngeal occlusion
    • Mixed apnea (most frequent in preterm infants)
      • Obstructive apnea preceding (usually) or following central apnea

EPIDEMIOLOGY

  • Apnea occurs in 1:1,000 term infants.
  • Incidence of AOP is inversely proportional to GA. It occurs in <10% of neonates >34 weeks GA and in almost all neonates <28 weeks GA at birth.
  • Generally resolves by 43 weeks postmenstrual age

RISK FACTORS

  • Prematurity: most common cause of neonatal apnea
  • Age: within first 30 days of life
  • Infection: sepsis, meningitis, upper respiratory tract infections, urinary tract infections, necrotizing enterocolitis
  • Upper airway obstruction: micrognathia, macroglossia, choanal atresia
  • Hemodynamic conditions of decreased cerebral blood flow: cardiac arrhythmias, hypotension, shock
  • Maternal medications: magnesium sulfate, opiates, anesthesia, β-blockers, selective serotonin reuptake inhibitors (SSRIs)
  • Medications given to infant: prostaglandin, opioids, sedatives
  • CNS abnormalities: seizure, hemorrhage, stroke, tumors
  • Anemia
  • Hypothermia or hyperthermia
  • Metabolic derangements: hypoglycemia, hypocalcemia, hyponatremia
  • Gastroesophageal reflux disease (GERD): Relationship is controversial.
  • Recent immunizations
  • Genetic conditions:
    • Heritability of AOP is reported to be 87% among same-sex twins.
    • Polymorphisms in adenosine A1 and A2 receptor genes.
    • PHOXB2 gene mutation causes congenital central hypoventilation syndrome (CCHS).

PATHOPHYSIOLOGY

  • Immature respiratory control in neonates
    • Immature structural development of central respiratory network in the brainstem
    • Enhanced sensitivity to inhibitory neurotransmitters (e.g., γ-aminobutyric acid [GABA]) and neuromodulators (e.g., adenosine, serotonin, and prostaglandin) that can lead to apnea
    • Low functional residual capacity predisposing to hypoxia when short apneas occur
  • Hypoxic ventilatory depression
    • Increased peripheral chemoreceptor sensitivity, leading to more unstable breathing (e.g., periodic breathing) or decreased sensitivity, which prolongs apnea when it does occur
    • Transition from low oxygen fetal environment to relatively high oxygen extrauterine environment can be interpreted by carotid body receptors as hyperoxia and trigger 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 gastroesophageal reflux (GER) can result in apnea, bradycardia, and hypotension.
    • More commonly, apnea events are preceded by GER events.
  • Pulmonary stretch receptors: exaggerated inhibitory response to stimulation of airway receptors
  • Sleep state: Neonates spend majority of their time in active, rapid eye movement (REM) sleep. Apneas are more common during REM sleep when breathing is irregular and chest wall and upper airway muscles are inactivated.
  • Upper airway obstruction: Hypotonic pharynx in preterm infants with additional loss of upper airway tone during active sleep leads to pharyngeal collapse and obstructive apnea.

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