APNEA

THUY L. NGO, DO, MEd AND SUSAN B. TORREY, MD

Neonates and infants can experience apneic episodes in response to a variety of physiologic and pathophysiologic processes not seen later in life. Differences in maturity of the central nervous system (CNS), respiratory drive and reserve, and susceptibility to infectious agents are among the factors that interact to make the very young patient susceptible. The causes of apnea in older children are similar to those in adults, although, those in infants and younger children, are different. In this chapter, the neonate and the young infant are emphasized, but for completeness, the older child also is considered.

Apnea is defined as a respiratory pause of greater than 20 seconds, or of any duration if there is associated pallor or cyanosis and/or bradycardia. Apnea must be distinguished from periodic breathing, which is a common respiratory pattern in young infants and is characterized by cycles of short respiratory pauses followed by an increase in respiratory rate. Normal newborn infants display respiratory patterns that vary by gender and by conceptual age, as well as by sleep state. Studies have demonstrated that premature infants typically have more apneic episodes than do term infants. Normal-term infants experience significantly more episodes of nonperiodic apnea during rapid eye movement (REM) sleep than during non-REM sleep, although respiratory failure occurs more often during non-REM sleep. Apnea can occur in the setting of an acute life-threatening event (ALTE), in which the apneic episode is accompanied by change in color, muscle tone, or mental status, or by choking.

PATHOPHYSIOLOGY

Respiratory centers in the pons and medulla control respiration through output to the upper airway and bellows apparatus. Peripheral modulators of respiration include hypoxia, hypercarbia, and laryngochemical stimulation. The immature response of the neonate and infant to these influences, in comparison to that of the older child, accounts for some of the vulnerability of these young patients. The adult response to hypoxemia is to increase respiratory rate in proportion to the decrease in oxygen partial pressure (PO₂). Tachypnea is maintained for the duration of the hypoxic stimulus. In contrast, the neonate demonstrates a brief increase in respiratory rate followed by depression of respiratory drive and, often, apnea. As an example, hypoxemia during sleep may not cause arousal in infants. Hypoxemia also results in less of a response to rising arterial carbon dioxide tension (PaCO₂) with further depression of respiratory drive. Therefore, mildly hypoxic infants tend to breathe periodically or develop apneic spells.

Feeding affects ventilation in young infants. Poor coordination of sucking and breathing can result in apnea. Furthermore, infants can develop apnea with hypoxia and bradycardia as the result of exaggerated laryngeal chemical reflexes and laryngospasm in response to regurgitation. Mild hypoxia, as can occur in association with feeding or sleep, exacerbates this response.

A number of exogenous factors, including toxins and metabolic derangements, affect respiratory control by causing medullary depression. Clinical experience demonstrates that newborns and very young infants are particularly sensitive to these factors; for example, hypoglycemia can be manifested as apnea in young infants, and apnea can be related to anemia in premature babies. The young infant is susceptible to bellows failure on a purely mechanical basis. The infant’s thoracic cage is extremely pliable, which can cause the chest wall to collapse during inspiration. More muscular effort is then required to produce an adequate tidal volume, resulting in increased work of breathing. In addition, the diaphragmatic muscles have limited glycogen stores and tire easily, resulting in greater vulnerability to respiratory failure as a result of respiratory distress.

DIFFERENTIAL DIAGNOSIS

The differential diagnosis of apnea is extensive (Table 9.1). Gastroesophageal reflux is frequently diagnosed in infants with an apparent life-threatening event (ALTE), with or without a history of vomiting. Several infectious processes can cause apnea. Meningitis, even in the absence of fever, must be included in the differential diagnosis. Respiratory syncytial virus, the predominant cause of bronchiolitis, may cause apnea in infants who were premature or have preexisting lung disease or congenital heart disease. Pertussis can cause apnea in small infants. Infant botulism is a diagnosis that will hopefully be made before apnea occurs. It must be suspected on the basis of age, symptoms, and clinical findings. Apnea may be the only clinical manifestation of seizure activity. This may be particularly difficult for emergency physicians to identify if they did not witness the episode and neurologic examination may be normal in the postictal period. Apnea may be a symptom of several systemic disease processes, including metabolic abnormalities that result in hypoglycemia, and sepsis. Congenital abnormalities must always be considered in newborns and in young infants. Prolongation of the QT interval can cause a dysrhythmia that is manifested as an ALTE. Finally, there have been well-substantiated reports of ALTE as the result of life-threatening child abuse such as Munchhausen’s by proxy or inflicted head injury. Frequently, no cause for the ALTE is identified.

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