APNEA DEL RECIEN NACIDO

Pathogenesis, clinical presentation, and diagnosis of apnea of prematurity

Apnea of prematurity is a developmental disorder in preterm infants that occurs as a direct consequence of immature respiratory control.

●Apnea of prematurity is most widely defined as cessation of breathing for more than 20 seconds or a shorter respiratory pause associated with oxygen desaturation and/or bradycardia in infants who are younger than 37 weeks gestation.

Apnea is classified as central, obstructive, or mixed depending upon the presence of continued inspiratory effort and upper airway obstruction while respiratory airflow is absent. In preterm infants, most apnea spells are classified as either being central or mixed. 

●The incidence of apnea is inversely proportional to gestational age (GA), and almost all extremely low birth weight (ELBW) infants (GA <28 weeks) are affected. 

●Although the exact mechanisms underlying apnea of prematurity are unknown, it is thought to be due to disruption of ventilation control processes due to immaturity that results in impaired central respiratory drive and/orinability to maintain upper airway patency. 

●Apnea of prematurity typically presents within the first few days of life in affected preterm infants who are not mechanically ventilated. It typically resolves before 37 postmenstrual weeks in infants delivered after 28 weeks gestation, but in infants born before 28 weeks, apnea frequently persists until 43 weeks postmenstrual age (PMA). (See 'Clinical presentation' above.)

●The diagnosis of apnea of prematurity is considered when either cessation of breathing greater than 20 seconds or a shorter period of respiratory pause accompanied by oxygen desaturation and/or bradycardia is detected. These events are typically identified by the routine use of cardiorespiratory monitors and/or pulse oximeters for preterm infants in the neonatal intensive care unit (NICU). Although apnea of prematurity is the most common cause of apnea in preterm infants, it is a diagnosis of exclusion. Other causes of apnea need to be considered and eliminated before the diagnosis of apnea of prematurity is made. 

●The goal of the diagnostic evaluation is to identify any underlying cause (eg, sepsis). The evaluation is based on a comprehensive history and assessment of the infant, and laboratory testing. 

Corte sagital de la vía aérea superior, mostrando colapso y la dilatación de las fuerzas ejercidas sobre la faringe durante la respiración normal

Management of apnea of prematurity

The management of apnea of prematurity typically includes supportive care, continuous positive airway pressure (CPAP), and caffeine therapy.

●We recommend initial cardiorespiratory monitoring for all preterm infants admitted to a neonatal intensive care unit (NICU), as they are at risk for apnea (Grade 1B).

●Supportive care is focused on eliminating factors that increase the risk of apnea. It includes maintenance of a stable thermal environment and nasal patency, avoidance of extreme neck flexion and extension, and identifying any other underlying condition associated with apnea (eg, sepsis). 

●In preterm infants with apnea, we suggest the use of nasal continuous positive airway pressure (nCPAP) (Grade 1C). Positive airway pressure reduces the risk of upper airway collapse and obstruction, and increases oxygenation. In these patients, positive airway pressure is begun at a pressure between 4 and 6 cm H2O via nasal prongs or mask.

●For infants with apnea of prematurity who require repeated tactile stimulation or ventilatory support, we recommend additional treatment with methylxanthine therapy versus general measures alone (Grade 1B). We recommend the use of caffeine rather than theophylline as the preferred methylxanthine for infants with apnea of prematurity (Grade 1B). Caffeine is the preferred agent because of its longer half-life and wider safety margin associated with a lower incidence of adverse effects. (See 'Caffeine versus theophylline' above.)

●Caffeine is given as a loading dose of 20 mg/kg of caffeine citrate (equivalent to 10 mg/kg caffeine base). It is followed in 24 hours by a daily maintenance dose of 5 to 10 mg/kg per dose (equivalent to 2.5 to 5 mg/kgcaffeine base). Both the loading and maintenance doses can be administered intravenously or orally. 

●We and other centers will frequently administer prophylactic caffeine therapy in extremely low birth weight (ELBW) infants (BW below 1000 g) to avoid intubation and mechanical ventilation, or to enhance extubation. 

●We suggest red blood cell (RBC) transfusions for infants with hematocrits of less than 25 to 30 percent who have frequent and/or severe apnea requiring intervention (Grade 2C).

●In our center, discontinuation of caffeine is considered for infants at a postmenstrual age (PMA) between 32 and 34 weeks who have a five-day period that is free of any apnea, bradycardia, or desaturation alarm event episode. 

●If an infant is ready for discharge, but mild apnea (ie, apneic episodes greater than 15 seconds that do not require intervention or are not accompanied with bradycardia and desaturation) continues to be a concern, home cardiorespiratory monitoring may be considered until the infant is 43 to 44 weeks PMA. Prior to discharge, the parents or primary home care provider must demonstrate proficiency in managing the monitor, providing stimulation, and performing cardiorespiratory resuscitation. Infants still exhibiting apnea with associated bradycardia or oxygen desaturation are not candidates for discharge and home monitoring.