Apnea of prematurity is defined as respiratory pauses > 20 sec or airflow interruption and respiratory pauses > 20 sec associated with bradycardia (< 80 beats/min), central cyanosis, or O2 saturation < 85% in neonates born at < 37 wk gestation and with no underlying disorders causing apnea. Cause may be CNS immaturity (central) or airway obstruction. Diagnosis is by multichannel respiratory monitoring. Treatment is with respiratory stimulants for central apnea and head positioning for obstructive apnea. Prognosis is excellent; apnea resolves in most neonates by 37 wk.
About 25% of preterm infants have apnea of prematurity, which usually begins 2 to 3 days after birth and only rarely on the first day. Apnea that develops > 14 days after birth in an otherwise healthy infant signifies a serious illness other than apnea of prematurity (eg, sepsis). Risk increases with earlier gestational age.
Apnea of prematurity may be
Central apnea is caused by immaturity of medullary respiratory control centers; insufficient neural impulses from the respiratory centers in the medulla reach the respiratory muscles, and the infant stops breathing. Hypoxemia and hypercarbia stimulate respiratory efforts.
Obstructive apnea is caused by obstructed airflow, neck flexion causing opposition of hypopharyngeal soft tissues, nasal occlusion, or reflex laryngospasm.
Both types of apnea can cause hypoxemia, cyanosis, and bradycardia if the apnea is prolonged. Among infants dying of SIDS, 18% have a history of prematurity, but apnea of prematurity does not seem to be a precursor to SIDS.
Although frequently attributable to immature respiratory control mechanisms, apnea of prematurity can be sign of major infectious, metabolic, thermoregulatory, respiratory, cardiac, GI, or CNS dysfunction. Careful history, physical assessment, and, when necessary, testing should be done before accepting prematurity as the cause of apnea.
Diagnosis of apnea usually is made by visual observation or by use of impedance-type cardiorespiratory monitors used continuously during assessment and ongoing care of preterm infants. Multichannel recordings of multiple physiologic parameters (eg, chest wall movement, airflow, O2 saturation, heart rate, brain electric activity) taken for up to 24 h can be used as adjuncts for diagnosis and planning and monitoring treatment.
Most preterm infants stop having apneic spells by the time they reach about 37 wk gestation. Apnea may continue for weeks in infants born at extremely early gestational ages (eg, 23 to 27 wk). Death is rare.
When apnea is noted, either by observation or monitor alarm, infants are stimulated, which may be all that is required; if breathing does not resume, bag-valve-mask or mouth-to-mouth-and-nose ventilation is provided (see Respiratory Arrest: Airway and Respiratory Devices). For infants at home, the physician is contacted if apnea occurs but ceases after stimulation; if intervention beyond stimulation is required, the infant should be rehospitalized and evaluated.
Frequent or severe episodes should be quickly and thoroughly evaluated, and identifiable causes should be treated. If no infectious or other treatable underlying disorder is found, respiratory stimulants are indicated for treatment of frequent or severe episodes, characterized by hypoxemia, cyanosis, bradycardia, or a combination. Caffeine is the safest and most commonly used respiratory stimulant drug. It can be given as caffeine base (loading dose 10 mg/kg followed by a maintenance dose of 2.5 mg/kg po q 24 h) or caffeine citrate, a caffeine salt that is 50% caffeine (loading dose 20 mg/kg followed by a maintenance dose of 5 to 10 mg/kg q 24 h). Caffeine is preferred because of ease of administration, fewer adverse effects, larger therapeutic window and less need to monitor drug levels. Treatment continues until the infant is 34 to 35 wk gestation and free from apnea requiring physical intervention for at least 5 to 7 days. Monitoring continues until the infant is free of apnea requiring intervention for 5 to 10 days.
If apnea continues despite respiratory stimulants, the infant may be given continuous positive airway pressure starting at 5 to 8 cm H2O pressure. Intractable apneic spells require ventilator support. Discharge practices vary; some practitioners observe infants for 7 days after treatment has ended to ensure that apnea or bradycardia does not recur, whereas others discharge with caffeine if treatment seems effective.
Hospitalized high-risk infants who have not had clinically significant cardiopulmonary events (eg, apnea > 20 sec, apnea accompanied by central cyanosis, apnea associated with heart rate < 80 for > 5 sec) during continuous cardiorespiratory monitoring can be discharged home safely without a monitor. A home cardiorespiratory monitor may be prescribed to shorten the hospital stay for infants that are otherwise ready for discharge but are still having clinically significant cardiopulmonary events that reverse without intervention. Caffeine can be used as an adjunct to a home monitor to achieve this status. Parents should be taught how to properly use equipment, assess alarm situations, intervene (eg, CPR), and keep a log of events. Round-the-clock telephone support and triage as well as outpatient follow-up regarding the decision to stop using the monitor should be provided. Monitors that store event information are preferred.
Infants should sleep on their back. The infant's head should be kept in the midline, and the neck should be kept in the neutral position or slightly extended to prevent upper airway obstruction. All premature infants, especially those with apnea of prematurity, are at risk of apnea, bradycardia, and O2 desaturation while in a car seat and should undergo a car seat challenge test before discharge.
Last full review/revision March 2009 by Anand D. Kantak, MD; John T. McBride, MD
Content last modified February 2012