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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 infants 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 1st day; apnea that develops > 14 days after birth in an otherwise healthy infant signifies a serious illness other than apnea of prematurity. Risk increases with earlier gestational age.
Etiology
and Pathophysiology
Apnea of prematurity may be central, obstructive, or both; a mixed pattern is most common. 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 briefly stimulates respiratory efforts but, after a few seconds, suppresses respirations. Obstructive apnea is caused by obstructed airflow, either from neck flexion causing opposition of hypopharyngeal soft tissues or from nasal occlusion. 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 appear to be a precursor to SIDS.
Diagnosis
Diagnosis of apnea itself is occasionally made by observation alone, but high-risk infants are typically diagnosed by an apnea monitor worn for 5 to 7 days. Typical monitors use a chest band to detect chest wall movements and pulse oximetry to detect heart rate and O2 saturation; nasal airflow must also be monitored if obstructive apnea is suspected. Apnea of prematurity is a diagnosis of exclusion. Other causes of apnea in neonates include hypoglycemia, hypocalcemia, sepsis, intracranial hemorrhage, and gastroesophageal reflux; these causes are sought with appropriate testing (see elsewhere in The Manual).
High-risk infants who are not apneic and who are otherwise ready for discharge may be monitored at home. Parents need to be taught how to place the monitoring belt and leads; how to interpret the significance of alarms by assessing the infant's color and respirations; and how to intervene. They should also be instructed to keep a log of alarms and infant appearance and to contact medical providers if questions arise or apneic episodes occur. Many monitors store information, allowing providers to assess the type and frequency of events, compare them with events reported and logged by the parents, and determine if other treatment is needed or if monitoring can be stopped.
Prognosis
and 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). Mortality, treated or untreated, is probably negligible.
The infant's head should be kept in the midline and the neck 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.
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 and Cardiac Arrest: Airway and Respiratory Devices). For infants at home, the physician is contacted if apnea occurred but ceased after stimulation; if intervention beyond stimulation is required, the infant should be rehospitalized and evaluated.
Respiratory stimulants are indicated for treatment of frequent or severe episodes, characterized by hypoxemia, cyanosis, and/or bradycardia. Caffeine is the safest and most commonly used 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 which is 50% caffeine (loading dose 20 mg/kg followed by a maintenance dose of 5 mg/kg q 24 h). Other options include IV methylxanthines ( aminophylline loading dose 6 to 7 mg/kg infused over 20 min followed by a maintenance dose of 1 to 3 mg/kg q 8 to 12 h [lower in younger, more premature infants] or theophylline loading dose 4 to 5 mg/kg followed by a maintenance dose of 1 to 2 mg/kg q 8 to 12 h), with doses adjusted to maintain a serum concentration of 6 to 12 μg/mL, and doxapram (0.5 to 2.0 mg/kg/h continuous IV infusion). Treatment continues until the neonate is 34 to 35 wk gestation and free from apnea requiring physical intervention for at least 5 to 7 days. Monitoring continues until the neonate is free of apnea requiring intervention for 5 to 10 days.
If apnea continues despite respiratory stimulants, the neonate 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 providers observe infants for 7 days after treatment has ended to ensure that apnea or bradycardia does not recur, whereas others discharge with theophylline if treatment appears effective.
Last full review/revision November 2005
Content last modified November 2005
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