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I. PROBLEM

An infant has just had an apneic episode with bradycardia (often referred to as “A’s and B’s”). American Academy of Pediatrics (AAP) has defined apnea as follows: “Apnea is the absence of breathing for 20 seconds or longer or a shorter pause associated with bradycardia (<100 beats per minute), cyanosis, or pallor.” Shorter apnea <10 seconds without hypoxemia or bradycardia is usually due to immaturity and is not clinically important. (See also Chapter 89.)

  1. The 3 types of apnea with approximate incidence are:

    1. Central apnea. Complete absence of the brainstem stimulus to breathe, resulting in no respiratory effort (10%–25%). Preterm infants can have central apnea due to their immature brains. Other causes include: inborn errors of metabolism, metabolic issues (hypoglycemia, hypocalcemia, acidosis), congenital anomalies, CNS infections, birth asphyxia, head trauma, toxin exposure.

    2. Obstructive apnea. Infant breathes but no airflow is present because of an obstruction usually at the pharyngeal level by mucus or airway collapse (10%–20%). Preterm infants have an increase in obstructive apnea due to difficulty maintaining their airway as a result of positioning.

    3. Mixed apnea. Elements of both central and obstructive apnea. Mixed apnea involves a period of central apnea usually followed by airway obstruction or vice versa. This is the most common type found in most premature infants (50%–75%). Other causes include gastroesophageal reflux, pertussis, and bronchiolitis.

  2. Definitions

    1. Apnea of infancy. The AAP definition of apnea of infancy (AOI) is as follows: “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 an infant >37 weeks’ gestational age at the onset of the apnea. It occurs in 1 per 1000 infants. AOI and apnea in term infants are interchangeable terms. Apnea in a term infant is not common and is usually pathologic and secondary to a long list of causes (eg, infection, seizure disorder, severe birth asphyxia, stroke, drug depression, intracranial hemorrhage, cerebral infarction, polycythemia, micrognathia).

    2. Apnea of prematurity. AAP defines apnea of prematurity (AOP) as follows: “Sudden cessation of breathing that lasts for at least 20 seconds or is associated with bradycardia or oxygen desaturation (cyanosis) in an infant <37 weeks’ gestational age.” It may start as obstructive or central but involves elements of both and is most commonly mixed apnea. AOP is a developmental disorder usually of physiologic immaturity of respiratory control, but other diseases may contribute. Factors found in the pathogenesis of AOP include central mechanisms and peripheral reflex pathways. Central mechanisms include decreased central chemosensitivity, hypoxic ventilatory depression, upregulated inhibitory neurotransmitters, and delayed central nervous system development. Peripheral reflex pathways include decreased or increased carotid body activity, laryngeal chemoreflex, and excessive bradycardic response. The incidence of AOP is inversely correlated with gestational age and birthweight. It affects almost all infants born ≤28 weeks of gestation or with a birthweight <1000 g. AOP may be hereditary. AOP usually presents on days 2 to 7. It usually resolves by 36 to 37 weeks of postmenstrual age (PMA) in 92% of infants born at ≥28 weeks’ gestation and by 40 weeks of PMA in >98% of infants. Infants born at <28 weeks’ gestation can have apnea to or beyond term gestation. If apnea presents in the first 24 hours of life or after day 7, it is very unlikely to be AOP. Note: AOP is a diagnosis of exclusion.

    3. Persistent apnea. Apnea that persists in a neonate ≥37 weeks of PMA. It usually occurs in infants born at <28 weeks’ gestation.

    4. Extreme apnea event. AAP defines this as apnea >30 seconds and/or heart rate <60 beats/min for >10 seconds.

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