Apnea of prematurity

Apnea of prematurity is defined as respiratory pauses of more than 20 s or interruption of airflow and respiratory pauses of less than 20 s, combined with bradycardia (less than 80 bpm), central cyanosis, or O2 saturation less than 85% in infants born at gestation less than 37 weeks and in the absence of causes that cause apnea. Causes of apnea of prematurity may include CNS (central) immaturity or airway obstruction.

Diagnosis is made by multichannel respiratory monitoring. Treatment is with respiratory stimulants for central apnea and correct head positioning for obstructive apnea. The prognosis is favorable; apneas cease in most newborns by 37 weeks.

About 25% of premature babies have apnea of prematurity, which usually begins 2-3 days after birth and very rarely on the first day; apnea that develops more than 14 days after birth in an otherwise healthy baby indicates a serious condition other than apnea of prematurity. The risk is greater the younger the gestational age.

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Causes of Apnea of Prematurity

Apnea of prematurity may be central, obstructive, or a combination of both; the mixed type is most common. Central apnea is caused by immaturity of the respiratory centers in the medulla oblongata; insufficient nerve impulses from the respiratory centers reach the respiratory muscles, and the child stops breathing. Hypoxemia briefly stimulates breathing, but depresses it after a few seconds. Obstructive apnea is caused by obstruction of the airway or by flexion of the neck, causing compression of the subpharyngeal soft tissues, or by impaired nasal breathing. Both types of apnea can cause hypoxemia, cyanosis, and bradycardia if the apnea is prolonged. Among children who died from SWS, 18% had a history of prematurity, but apnea of prematurity was not found to precede SWS.

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Diagnosis of apnea of prematurity

The diagnosis of apnea itself is made incidentally based on observation of the infant, but in high-risk infants an apnea monitor is used for 5 to 7 days. Typical monitors have a band around the chest to detect chest movement and a pulse oximeter to determine heart rate and O2 saturation; nasal breathing should 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 identified with appropriate testing.

High-risk infants who do not have apnea and are ready for discharge may continue monitoring at home. Parents should be taught how to place the belt and leads; how to interpret the significance of alarms by assessing the infant's skin color and breathing; and how to assist the infant if needed. They should also be instructed in how to keep an alarm diary and how to contact the health care provider if questions arise or if the infant experiences apneic episodes. Many monitors store information, allowing the health care provider to evaluate the type and frequency of episodes, compare them with those reported and recorded by the parent, and determine whether other treatment is needed or the monitor can be removed.

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Treatment of apnea of prematurity

The infant's head should be positioned in the midline and the neck should be in a neutral or slightly extended position to avoid upper airway obstruction. All premature infants, especially those with apnea of prematurity, are at high risk for apnea, bradycardia, and O2 desaturation while in a car seat and should undergo a car seat test before discharge.

If apnea is noted either by observing the child or by a signal from the monitor, the child should be irritated, this may be sufficient; if breathing is not restored, artificial ventilation is performed by bag-valve-mask or mouth-to-mouth and nose. If children are at home, the doctor should be contacted if apnea occurs that disappears with irritation; if other types of intervention are required, the child should be readmitted and examined.

Respiratory stimulants are indicated for frequent or severe episodes characterized by hypoxemia, cyanosis, and/or bradycardia. Caffeine is the safest and most commonly used agent. It can be given as the base (initial dose of 10 mg/kg, then maintenance dose of 2.5 mg/kg orally after 24 hours) or as the citrate salt of caffeine containing 50% caffeine (initial dose of 20 mg/kg, then maintenance dose of 5 mg/kg after 24 hours). Other options include intravenous methylxanthines [aminophylline (initial dose 6-7 mg/kg over 20 minutes, then maintenance dose 1-3 mg/kg at 8-12 hours (lower in younger, more premature infants) or theophylline (initial dose 4-5 mg/kg, then maintenance dose 1-2 mg/kg at 8-12 hours), titrated to maintain blood theophylline levels of 6-12 mcg/mL, and doxapram (0.5-2.0 mg/(kg × hr) continuous intravenous infusion). Treatment is continued until the infant reaches 34-35 weeks' gestation and has had at least 5-7 days of apnea requiring intervention. Monitoring continues until he has had at least 5-10 days of apnea requiring intervention.

If apnea continues despite respiratory stimulants, the infant may be placed on ventilator support starting at 5-8 cm H2O. Unrelieved episodes of apnea require ventilation. The decision to discharge the infant varies among physicians; some physicians monitor the infant for 7 days after treatment to ensure that apnea or bradycardia does not recur, while others discharge infants on theophylline if the treatment is effective.

Prognosis of apnea of prematurity

Most premature infants stop having apneic episodes by the time they reach approximately 37 weeks of gestation; apnea may continue for weeks in infants born at extremely early gestation (23–27 weeks). Mortality from apnea of prematurity is low and is not affected by treatment.