Introduction

Apnea is defined as pauses in breathing for 5 to 10 seconds and is often pathologic after pauses of 20 seconds or greater.¹ The American Academy of Pediatrics defines apnea 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 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 as obstructive, 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 stimulation 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 gestational 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 new-onset apnea episodes 7 days after a previous episode require evaluation for other causes of apnea including anemia, infection, and electrolyte disturbances.¹⁰

Diagnosis

AOP is a diagnosis of exclusion. All causes of apnea in a neonate should be evaluated prior to initiating treatment therapies. Potential causes of apnea are provided in Table 6-1. Physical assessment, laboratory monitoring, and patient history should be evaluated to rule out secondary causes of apnea.

Physical assessment includes

•temperature

•respiratory evaluation

Laboratory monitoring includes

•complete blood cell count (white blood cells with differential, red blood cells, and platelets) assessing for potential infectious or anemic causes

•metabolic panels (electrolytes and glucose) evaluating potential metabolic disorders and arterial blood gases evaluating oxygenation status^11–13

Patient and maternal histories provide information on possible medication exposures and infection risks.

Goals of Therapy

Limiting or eliminating apnea episodes lasting over 20 seconds or episodes resulting in bradycardia or cyanosis is the principal goal of therapy when treating AOP. Treatment, either nonpharmacologic or pharmacologic, is required with increased frequency and prolonged apnea episodes or episodes that result in bradycardia or hypoxemia.¹⁴ Typically, both treatment modalities are used in combination to achieve therapeutic goals.

Treatment Therapies

Nonpharmacologic Treatments

Nonpharmacologic treatments are often initiated prior to starting or in combination with pharmacologic options. Nonpharmacologic treatment options include manual stimulation, airway patency maintenance, red blood cell transfusions, supplemental oxygen therapy, and respiratory support.

Manual stimulation is a first step used by a member of the healthcare team when a neonate is experiencing an acute apneic event. The neonate is stimulated by the healthcare team member rubbing on the neonate’s chest, back, or extremities prompting spontaneous breathing.

Airway patency can be compromised by neonatal patient positioning and instrumentation. Neck positioning may lead to obstruction of the airway. Limiting extension and flexion of the neck decreases risk of apnea due to obstruction.⁸ Instrumentation may also obstruct the airway, leading to apneic episodes. Nasogastric tubes may hinder airflow.

Hypoxemia is a cause of apnea. Decreasing hypoxemia decreases risk of apnea. Two options to reduce hypoxemia are transfusing red blood cells to increase the neonate’s ability to deliver oxygen to the body and providing supplemental oxygen to increase the oxygen saturation. Both nonpharmacologic options preventing hypoxemia have potential risks resulting in other neonatal conditions, such as retinopathy of prematurity and necrotizing enterocolitis. (See Chapters 1 and 13 for discussions.) Blood transfusions in moderately anemic neonates did not decrease duration, severity, or frequency of apnea episodes.¹⁵ Oxygen saturation goals for neonates at risk for retinopathy of prematurity, including neonates with AOP, remain unclear. Supplemental oxygen may not exacerbate threshold retinopathy of prematurity.¹⁶

Respiratory ventilation support such as continuous positive airway pressure (CPAP) helps with obstructive components of apnea by splinting the upper airway open to maintain patency.¹⁷ CPAP also increases functional residual capacity, prolonging time from apnea to desaturations, and ultimately time to bradycardia.⁷ When neonates continue to experience apneic episodes after CPAP and pharmacologic therapy maximization, endotracheal intubation may be required to limit episodes.⁸

Pharmacologic Treatments

For over 25 years the pharmacologic treatment class of choice is methyl-xanthines—aminophylline, caffeine, and theophylline. Efficacy is similar between the three agents.^18,19 Caffeine is the medication of choice in practice due to a favorable adverse event profile, wide therapeutic index, and administration advantages.^20,21

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