6 Apnea of Prematurity John Brock Harris, PharmD, BCPS, BCPPS Introduction pnea is defined as pauses in breathing for 5 to 10 seconds and is often pathologic after pauses of A 1 20 seconds or greater. The American Acade- my of Pediatrics definesapnea of prematurity (AOP) as a “cessation of breathing for at least 20 seconds or as a briefer episode of apnea associated with bradycardia, cyanosis, or pallor.”2 AOP treatment is required to prevent short- and long-term adverse outcomes. Epidemiology Young gestational age and extremely low birth weight neonates have increased 66 NICU PRIMER FOR PHARMACISTS incidences of AOP. Seven percent of neonates born at 34 weeks gestation or older and 80% of neonates with a birth weight under 1 kilogram (kg) experience apnea.3,4 Apnea may be classified asobstructive , central, or mixed. Mixed apnea represents greater than 50% of episodes followed by central and obstructive apneas.5 Pathophysiology Obstructive apnea is related to decreased airflow with functioning breathing mechanics (chest wall motion). Central apnea is related to decreased stimula- tion from the central nervous system (CNS) to the respiratory musculature. Both airflow and breathing mechanics are deficient in central apnea.Mixed apnea has components of both obstructive and central apneas. Obstructive apnea typically results from pharyngeal collapse caused by either upper airway muscle inability to maintain patency of airway or negative pressures produced during inhalation.6 The obstruction location may also be in the larynx or a combination of the pharynx and larynx. Central apnea is directly correlated with brainstem maturity; specifically, it is related to functional maturity based on delayed neuronal conduction and not anatomic maturity.7 The more immature a neonate’s brainstem, the more likely the patient will experience central apnea. The brainstem respiratory center in early gesta- tional age neonates also has a decreased response to carbon dioxide, leading to apnea instead of hyperventilation as in older patients.6 AOP consists of pauses in respiratory airflow for 5 to more than 20 seconds. After 20 seconds of apnea, neonates become hypoxemic. This leads to the patient becoming cyanotic and bradycardic. Airflow pauses greater than 30 seconds lead to hypotonia and pallor. AOP usually resolves by 36 weeks’ postconception.6 Presentation Experts recommend that neonates younger than 35 weeks’ gestation should be monitored during the first 7 days of life for AOP.8 Within the first 48 hours of life, premature neonates with no mechanical respiratory support commonly present with apneic episodes. Neonates who require mechanical support may not experience apneic episodes until after support has been weaned or discontinued.9 Patients requiring no mechanical support who have delayed episodes of apnea after the first 7 days of life or experience .