bubble_chart Overview

Many premature infants ≤34 weeks experience apnea, which typically occurs within 2–3 days after birth. The incidence increases with decreasing gestational age. Pathological factors include hypoglycemia, hypocalcemia, sepsis, intracranial hemorrhage, and occasionally gastroesophageal reflux. Therefore, premature infants with apnea should undergo thorough evaluation to rule out these treatable underlying conditions.

Periodic breathing (rapid breathing with pauses) results from immaturity of the medullary respiratory center. Apnea is defined as a pause in respiration lasting more than 20 seconds. Hypoxemia and bradycardia may occur, requiring intervention to stimulate breathing. Neonatal hypoxemia initially stimulates respiration transiently but suppresses it after a few seconds.

The distinction between central and obstructive apnea lies in the mechanism: central apnea occurs due to insufficient neural impulses from the medullary respiratory center to the respiratory muscles, causing the infant to stop breathing.

Upper airway obstruction (obstructive apnea) results from blockage of airflow due to collapse of pharyngeal soft tissues. The infant struggles to breathe but cannot draw air into the lungs, rapidly leading to hypoxemia and bradycardia. Because chest wall movements persist, obstructive apnea may not be detected by impedance apnea monitors, but nasal airflow monitoring reveals the absence of airflow.

Low-birth-weight infants are at risk for apnea and require monitoring of respiration and heart rate, as well as pulse oximetry to measure oxygen saturation. If apnea, bradycardia, or desaturation occurs, nurses must intervene immediately.

bubble_chart Treatment Measures

The infant should lie flat, with the head in the midline position and the neck in a natural or slightly extended posture to prevent upper airway obstruction. If apnea episodes persist, especially when accompanied by cyanosis and bradycardia, aminophylline can be used for treatment (dose refer to the prognosis and treatment of respiratory distress syndrome mentioned above). If the infant begins feeding, the same dose of theophylline can be administered orally or via gastric tube. Alternatively, the infant can be switched to a coffee bean solution (loading dose of 10 mg/kg, maintenance dose of 5 ml/kg per day), as coffee bean has stronger therapeutic indications and fewer side effects compared to aminophylline. Another respiratory stimulant is doxapram, with a dose of 0.5–2 mg/kg administered via continuous intravenous infusion, though experience with this drug in premature infants is limited.

If apnea persists despite the use of respiratory stimulants, the infant can be treated with CPAP via nasal cannula or endotracheal tube, starting at a pressure of 5–8 mmH₂O. Refractory apnea may require ventilator support.

Treatment with methylxanthines (aminophylline, theophylline, or coffee bean) should be discontinued 7 days after the cessation of apnea episodes in the infant. The infant can be discharged home 7 days after stopping methylxanthines if no apnea or bradycardia occurs. Many premature infants stop experiencing apnea once they reach a gestational age of 37 weeks. However, apnea or bradycardia may persist for weeks in very preterm newborns (e.g., gestational age of 23–27 weeks). A 24-hour respiratory recording may help assess episodes of apnea, bradycardia, and hypoxia.

Parents who receive comprehensive training (including CPR equipment, assessment plans, and home support) can reduce the risk of life-threatening apnea episodes in their infant, eliminating the need for methylxanthine treatment and home monitoring. Home monitors will alarm if apnea lasts beyond a set limit (typically 15 seconds) or if the heart rate drops below a set threshold (usually 80–100 beats per minute). Batteries maintain functionality to prevent power depletion. Many monitors store data for later documentation and analysis, allowing physicians to determine the type and frequency of episodes and explain the condition to parents. This also helps assess whether additional treatment is needed or if monitoring can be discontinued.

Infants at high risk for sudden infant death syndrome (SIDS) are generally placed on home monitoring, and some infants with acute life-threatening conditions have been successfully resuscitated. However, some infants have died despite home monitoring. Therefore, the American Academy of Pediatrics has concluded that home monitoring does not prevent SIDS.