APNEA IN THE PRETERM INFANT
Saturday, August 16, 2008
Essentials of Diagnosis & Typical Features
In preterm infants, recurrent apneic episodes are a common problem. Apnea is defined as a respiratory pause lasting more than 20 seconds—or any pause accompanied by cyanosis and bradycardia. Shorter respiratory pauses associated with cyanosis or bradycardia also qualify as significant apnea but must be differentiated from periodic breathing, which is common in term as well as preterm infants. Periodic breathing is defined as regularly recurring ventilatory cycles interrupted by short pauses not associated with bradycardia or color change. Although apnea in premature infants is often not associated with a predisposing factor, a variety of processes may precipitate apnea (Table 1–20). These processes should at least be considered before a diagnosis of apnea of prematurity can be established.
Apnea of prematurity is the most frequent cause of apnea. Most apnea of prematurity is mixed apnea characterized by a centrally (brainstem) mediated respiratory pause preceded or followed by airway obstruction. Less common is pure central or pure obstructive apnea. Apnea of prematurity is the result of immaturity of both the central respiratory regulatory centers and protective mechanisms that aid in maintaining airway patency.
Clinical Findings
Onset, typically during the first 2 weeks of life, is gradual, with the frequency of spells increasing over time. Pathologic apnea can be suspected in an infant with a sudden onset of frequent or very severe apneic spells. Apnea presenting from birth or on the first day of life is unusual but can occur in the preterm infant who does not require mechanical ventilation for respiratory distress syndrome. In the term or near-term infant, this presentation can suggest neuromuscular abnormalities of an acute (asphyxia, birth trauma, or infection) or chronic (eg, congenital hypotonia, structural CNS lesion) nature.
The workup depends on the clinical presentation. All infants—regardless of the severity and frequency of apnea—require a minimum screening evaluation, including a general assessment of well-being (eg, tolerance of feedings, stable temperature, normal physical examination), a check of the association of spells with feeding, measurement of PaO2 or SaO2, blood glucose, hematocrit, and a review of the drug history. Infants with severe apnea of sudden onset may require a more extensive evaluation, including a workup for infection. Other specific tests are dictated by relevant signs, for example, evaluation for necrotizing enterocolitis in an infant with apnea and abdominal distention.
Treatment
The physician should first address any underlying cause. If the apnea is due simply to prematurity, treatment is dictated by the frequency and severity of apneic spells. Apneic spells frequent enough to interfere with other aspects of care (eg, feeding), or severe enough to necessitate bag and mask ventilation to relieve cyanosis and bradycardia, require treatment. First-line therapy is with methylxanthines. Caffeine citrate (20 mg/kg as loading dose and then 5–10 mg/kg/d) is the drug of choice because of once-daily dosing and fewer side effects than theophylline (5 mg/kg load; 1–2 mg/kg every 6–12 hours). Side effects of methylxanthines include tachycardia, feeding intolerance, and (with overdosing) seizures. The dose used should be the smallest dose necessary to decrease the frequency of apnea and eliminate severe spells. Desired drug levels are usually in the range of 5–10 µg/mL for theophylline and 10–20 µg/mL for caffeine. Intravenous doxapram infused at a dose of 1 mg/kg/h for 48 hours is effective in some cases of methylxanthine-refractory apnea. Nasal CPAP (continuous positive airway pressure), by treating the obstructive component of apnea, can be effective treatment for some infants. Intubation and ventilation can eliminate symptomatic apneic spells but carries the risks associated with long-term endotracheal intubation.
Prognosis
In the majority of premature infants, apneic and bradycardiac spells cease by 34–37 weeks postconception. The spells tend to disappear by degree of severity; spells that require intervention cease prior to self-resolved episodes. Occasionally the episodes last longer. In infants born at less than 28 weeks’ gestation, episodes may continue past term postconceptual age. Whether to provide home monitoring or outpatient methylxanthine therapy for such infants is controversial. Apneic and bradycardiac episodes in the nursery are not predictors of later SIDS. However, home monitoring in infants still experiencing self-resolving apnea and bradycardia at the time of hospital discharge may be indicated in some cases. The incidence of SIDS is slightly increased in preterm infants. Research in term infants has shown an increased incidence of SIDS in infants who sleep in the prone position. Whether this can be extrapolated to the preterm infant (in particular those with gastroesophageal reflux or persistent respiratory symptoms) is unclear. When possible, a sleeping position on the side (right side down) or, preferably, supine seems prudent unless contraindicated by reflux or respiratory symptoms.
- Respiratory pause of sufficient duration to result in cyanosis or bradycardia.
- Most common in infants born at less than 34 weeks’ gestation with onset at less than age 2 weeks.
- Methylxanthines (eg, caffeine) provide effective treatment for apnea of prematurity.
In preterm infants, recurrent apneic episodes are a common problem. Apnea is defined as a respiratory pause lasting more than 20 seconds—or any pause accompanied by cyanosis and bradycardia. Shorter respiratory pauses associated with cyanosis or bradycardia also qualify as significant apnea but must be differentiated from periodic breathing, which is common in term as well as preterm infants. Periodic breathing is defined as regularly recurring ventilatory cycles interrupted by short pauses not associated with bradycardia or color change. Although apnea in premature infants is often not associated with a predisposing factor, a variety of processes may precipitate apnea (Table 1–20). These processes should at least be considered before a diagnosis of apnea of prematurity can be established.
Apnea of prematurity is the most frequent cause of apnea. Most apnea of prematurity is mixed apnea characterized by a centrally (brainstem) mediated respiratory pause preceded or followed by airway obstruction. Less common is pure central or pure obstructive apnea. Apnea of prematurity is the result of immaturity of both the central respiratory regulatory centers and protective mechanisms that aid in maintaining airway patency.
Clinical Findings
Onset, typically during the first 2 weeks of life, is gradual, with the frequency of spells increasing over time. Pathologic apnea can be suspected in an infant with a sudden onset of frequent or very severe apneic spells. Apnea presenting from birth or on the first day of life is unusual but can occur in the preterm infant who does not require mechanical ventilation for respiratory distress syndrome. In the term or near-term infant, this presentation can suggest neuromuscular abnormalities of an acute (asphyxia, birth trauma, or infection) or chronic (eg, congenital hypotonia, structural CNS lesion) nature.
The workup depends on the clinical presentation. All infants—regardless of the severity and frequency of apnea—require a minimum screening evaluation, including a general assessment of well-being (eg, tolerance of feedings, stable temperature, normal physical examination), a check of the association of spells with feeding, measurement of PaO2 or SaO2, blood glucose, hematocrit, and a review of the drug history. Infants with severe apnea of sudden onset may require a more extensive evaluation, including a workup for infection. Other specific tests are dictated by relevant signs, for example, evaluation for necrotizing enterocolitis in an infant with apnea and abdominal distention.
Treatment
The physician should first address any underlying cause. If the apnea is due simply to prematurity, treatment is dictated by the frequency and severity of apneic spells. Apneic spells frequent enough to interfere with other aspects of care (eg, feeding), or severe enough to necessitate bag and mask ventilation to relieve cyanosis and bradycardia, require treatment. First-line therapy is with methylxanthines. Caffeine citrate (20 mg/kg as loading dose and then 5–10 mg/kg/d) is the drug of choice because of once-daily dosing and fewer side effects than theophylline (5 mg/kg load; 1–2 mg/kg every 6–12 hours). Side effects of methylxanthines include tachycardia, feeding intolerance, and (with overdosing) seizures. The dose used should be the smallest dose necessary to decrease the frequency of apnea and eliminate severe spells. Desired drug levels are usually in the range of 5–10 µg/mL for theophylline and 10–20 µg/mL for caffeine. Intravenous doxapram infused at a dose of 1 mg/kg/h for 48 hours is effective in some cases of methylxanthine-refractory apnea. Nasal CPAP (continuous positive airway pressure), by treating the obstructive component of apnea, can be effective treatment for some infants. Intubation and ventilation can eliminate symptomatic apneic spells but carries the risks associated with long-term endotracheal intubation.
Prognosis
In the majority of premature infants, apneic and bradycardiac spells cease by 34–37 weeks postconception. The spells tend to disappear by degree of severity; spells that require intervention cease prior to self-resolved episodes. Occasionally the episodes last longer. In infants born at less than 28 weeks’ gestation, episodes may continue past term postconceptual age. Whether to provide home monitoring or outpatient methylxanthine therapy for such infants is controversial. Apneic and bradycardiac episodes in the nursery are not predictors of later SIDS. However, home monitoring in infants still experiencing self-resolving apnea and bradycardia at the time of hospital discharge may be indicated in some cases. The incidence of SIDS is slightly increased in preterm infants. Research in term infants has shown an increased incidence of SIDS in infants who sleep in the prone position. Whether this can be extrapolated to the preterm infant (in particular those with gastroesophageal reflux or persistent respiratory symptoms) is unclear. When possible, a sleeping position on the side (right side down) or, preferably, supine seems prudent unless contraindicated by reflux or respiratory symptoms.
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