You are at your outpatient surgery center. You run in to see your last patient of the day. It’s a 3.5-month-old baby who is scheduled to have an inguinal hernia repair; this case should be a piece of cake! You are confused though when you see the baby. He is awfully little, weighing only 2.1 kg. Speaking with the mother, you find out that she has only had little Tommy at home for the last 2 weeks and that this hernia popped up 2 days ago. Tommy is so tiny because he arrived 14 weeks early. While talking to both the mother and the surgeons, you quickly calculate that he was born at 26 weeks gestation and that he is now just 40 weeks postconceptual age (26 weeks of gestational age plus 14 weeks of chronologic age). Except for the hernia, the mother says all is well. Use of the apnea monitor was discontinued just before Tommy went home. The surgeon says that the hernia needs to be fixed because it is hard to reduce. He asks you, “Can’t you just watch him for a couple of hours here then let them go home?” What should you do?

Idiopathic apnea occurs in up to 55% of infants born prior to 37 weeks of gestation and in up to 2% to 3% of full-term infants. All infants, especially those born prematurely, are at risk for postoperative apnea. It is crucial to identify those infants at increased risk for postoperative apnea in order to provide extended monitoring and intervention when necessary.

Apnea is defined as an unexplained pause in breathing lasting 15 to 20 seconds or one lasting less than 15 seconds when associated with bradycardia (heart rate <80), cyanosis, pallor, or marked hypotonia. There are three identifiable types of apnea. Central apnea is characterized by a lack of respiratory effort. Obstructive apnea exists when respiratory effort is present without airflow. Mixed apnea is a combination of both central and obstructive mechanisms.

The most common pattern of apnea in infants has a mixed etiology, withcentral apnea playing the predominant role. Infants, particularly those born prematurely, have an immature central nervous system that manifests as a decreased response to carbon dioxide and a paradoxic response to hypoxia, leading to apnea rather than hyperventilation. Other contributing factors to neonatal apnea include immature intercostal and diaphragmatic musculature, an unstable pliable rib cage, an easily obstructed upper airway, and a lower airway prone to collapse. The long-term consequences of apnea
are largely undefined. However, it is reasonable to conclude that hypoxemia associated with repeated apnea increases the likelihood of central nervous system damage.

Anesthesia accentuates a neonate’s propensity for apneic events. The first apneic spell can occur up to 12 hours postoperatively. Both inhalational and intravenous anesthetics alter respiratory function. Inhaled anesthetics compromise the infant’s immature central nervous system. They have been shown to reduce the central response to respiratory stimulants, including hypercarbia and hypoxia, and to enhance the response to inhibitory afferents. Furthermore, inhaled anesthetics relax pharyngeal musculature, promoting upper-airway obstruction in the neonate who is already prone to obstructive apnea. Intravenous anesthetics, including opioids, also depress the centralnervous-system respiratory centers.