APNEA OF PREMATURITY
Category: Child Health
Abstract : Apnea of Prematurity A fetus makes breathing movements from early in pregnancy, although the purpose of fetal breathing is unknown. Breathing is intermittent in the fetus and becomes continuous after birth. The mechanisms that cause the transition from intermittent fetal breathing to continuous neonatal breathing remain unelucidated. All premature neonates, as well as most full-term neonates, h
Apnea of Prematurity
A fetus makes breathing movements from early in pregnancy, although the purpose of fetal breathing is unknown. Breathing is intermittent in the fetus and becomes continuous after birth. The mechanisms that cause the transition from intermittent fetal breathing to continuous neonatal breathing remain unelucidated.
All premature neonates, as well as most full-term neonates, have apnea, which is defined as pauses in their breathing pattern. In most instances, this apnea is brief and causes no physiologic changes.
Definition and classifications of apnea of prematurity
Pathologic apnea is defined as apnea exceeding 20 seconds' duration or apnea of shorter than 20 seconds if it is accompanied by bradycardia or oxygen desaturation. Bradycardia in a premature neonate is considered significant when the heart rate slows at least 30 beats per minute (bpm) from the resting heart rate. An oxygen saturation level less than 85% is considered pathologic in this age group. In all cases, the decrease in saturation should persist for at least 5 seconds. These levels represent significant apnea, bradycardia, and oxygen saturation changes that rarely occur in healthy preterm neonates older than 36 weeks after conception.
Apnea is classified as central, obstructive, or mixed. Central apnea is defined as the cessation of both airflow and respiratory effort. Obstructive apnea is the cessation of airflow in the presence of continued respiratory effort. Mixed apnea contains elements of both central and obstructive apnea, either within the same apneic pause or at different times during a period of respiratory recording.
Apnea of infancy
Apnea of infancy (AOI) occurs when apnea persists in a neonate older than 37 weeks after conception. The physiologic aspects of apnea of prematurity (AOP) and AOI coincide, although further studies are needed to determine the exact nature of their relationship.
Periodic breathing :
Periodic breathing (PB) is defined as periods of regular respiration for as long as 20 seconds followed by apneic periods no longer than 10 seconds that occur at least 3 times in succession (see Image 3). In most cases, PB accounts for 2-6% of the breathing time in healthy term neonates and as much as 25% of the breathing time in preterm neonates. PB occurrence is directly proportional to the degree of prematurity. Kelly and coworkers found that PB occurred in 78% of patients examined at age 0-2 weeks; the incidence declined significantly to 29% at age 39-52 weeks. This condition does not occur in neonates during their first 2 days of life.
PB is more frequent during active sleep, but it can occur when neonates are awake or quietly sleeping. This pattern, common at high altitudes, is eliminated with the administration of supplemental oxygen and/or with the use of continuous positive airway pressure (CPAP). Because the prognosis is excellent, no treatment is usually required.
apnea of prematurity Pathophysiology: Inspiration is controlled by an off switch. During inspiration, the augmenting discharge of the central inspiratory activator to the inspiratory motor neurons and specialized right bundle (Rb) neurons suddenly causes the off-switch neurons to discharge, transiently inhibiting the central inspiratory activator and allowing passive exhalation. Pulmonary volume sensors and the rostral pontine pneumotaxic center also control the off switch.
The pathophysiology of AOP has been attributed to abnormal breathing control caused by neuronal immaturity of the brainstem. This immaturity probably is secondary to decreased afferent traffic from peripheral receptors to the reticular formation. When dendritic and other synaptic interconnections multiply, breathing control improves as the brain matures, and AOP tends to resolve. This resolution typically occurs 34-52 weeks after conception.
Indomethacin stimulates phrenic neural output in an anesthetized piglet model; this finding supports the concept that prostaglandins inhibit breathing early in neonatal life. The final output of the respiratory control nuclei in the medulla may be a complex function of many inhibitory and stimulatory inputs, both humoral and neural. The exact manner in which these are altered during AOP remains unknown.
Sleep
Although determining the sleep state in neonates younger than 34 weeks is controversial, apnea appears to occur predominantly during active (ie, rapid eye movement [REM]) and indeterminate or transitional sleep in preterm and full-term neonates. Several mechanisms have been proposed to explain the high incidence of apnea during active sleep. Chest-wall movements are predominantly out of phase or paradoxical during active sleep, unlike their state during quiet sleep. A decrease in the fractional catabolic rate (FCR) and a decrease of 6-10 mm Hg in PaO2 have been observed in infants during active sleep, and both effects predispose an infant to apneic episodes. Moreover, ventilatory responses to increased carbon dioxide and decreased oxygen concentrations attenuate during active sleep.
Chemoreceptors
Preterm neonates respond to a decrease in the inspired oxygen concentration by transiently increasing the ventilation rate for approximately 1 minute and then returning to baseline or even depressed ventilation rates. A progressive decrease in the inspired oxygen concentration causes significant flattening of carbon dioxide responsiveness in preterm neonates. This unstable response to low concentrations of inspired oxygen may play an important role in the etiology of neonatal apnea. Central chemoreceptor activity is less developed in immature neonates younger than 33 weeks after conception. The sensitivity of the central chemoreceptor to CO2 is reduced in premature neonates and increases progressively with gestational age to adult levels by term. The sensitivity to CO2 is increased with higher O2 concentrations and decreased in hypoxemia.
The primary problem for premature neonates may be the relative weakness of the peripheral chemoreceptor function, at least during the first few weeks of life. The central hypoxic depression of ventilation, mediated by the midbrain inhibitor, also disappears about 2-3 weeks after birth when the mature response of sustained hypoxic stimulation of ventilation becomes dominant.
Upper airway
Reflexes originating from the upper airway may directly alter the pattern of respiration in infants and play a crucial role in initiating and terminating apnea. Sensory input from these upper airway receptors travels to the CNS through cranial nerves V, VI, IX, X, XI, and XII and may have powerful effects on the respiratory rate and rhythm, heart rate, and vascular resistance. These observations suggest that afferent sensory input from the upper airway is necessary for airway patency.
Adenosine
Adenosine and its analogues cause respiratory depression. Adenosine antagonism also has been proposed as a mechanism to explain the therapeutic effect of theophylline.
Oxygen
Inhalation of low oxygen concentrations produces an immediate 1-minute-long increase in the ventilation rate, followed by a 5-minute-long decrease. Infants with borderline hypoxia tend to breathe periodically or have apneic spells. These apneic spells, which are frequently associated with bradycardias, can be relieved by increasing the inspired oxygen concentration. Hypoxia also can induce PB in these infants.
Hering-Breuer reflex
The Hering-Breuer reflex (ie, inflation reflex) decreases the frequency of inspiratory effort during distension of the lungs. This effect is reflex-mediated via afferent vagal fibers. The Hering-Breuer reflex is more active in neonates than in adults, to the extent that small increases in lung volume may cause apnea.
Bradycardia
Bradycardias observed during apnea may result from chemoreceptor-induced inhibition of the heart rate in the absence of ventilatory effort.
Swallowing
AOP can be distinguished from PB by the frequent swallowing-like movements in the pharynx during the apnea. The etiology of swallowing during apnea is unknown.
Frequency:
• In the US: Although not always apparent, AOP is the most common problem in premature neonates. Approximately 70% of babies born at less than 34 weeks' gestation have clinically significant apnea, bradycardia, or oxygen desaturation during their hospitalization. Apnea is more frequent in less mature infants. Apnea may occur during the postnatal period in 25% of neonates who weigh less than 2500 g at birth and in 84% of neonates who weigh less than 1000 g. Carlo and associates have shown that apnea onset may occur on the first day of life in neonates without respiratory distress syndrome. AOP frequency rates may be as high as 50% in premature babies. An estimated 50% or more of surviving infants who weigh less than 1500 g at birth have apneic episodes that must be managed with ventilatory support or pharmacologic intervention.
Mixed apnea accounts for approximately 50-75% of all cases of apnea in premature neonates, 10-20% of obstructive apneas, and 10-25% of central apneas. In 50% of all apneic episodes, central apnea is either preceded or followed by an obstructive component and leads to mixed apnea.
• Internationally: To the author's knowledge, no data are available to compare the incidences of AOP in other countries.
Mortality/Morbidity: Butcher-Puech and coworkers found that infants in whom obstructive apnea exceeded 20 seconds in duration had a higher incidence of intraventricular hemorrhage, hydrocephalus, prolonged mechanical ventilation, and abnormal neurologic development after their first year of life. In 1985, Perlman and Volpe described a decrease in the cerebral blood flow velocity that accompanies severe bradycardia (ie, heart rate <80 bpm). Infants with significant AOP do not perform as well in neurodevelopmental follow-up testing as similar premature infants without recurrent apneas.
Race: No racial predilection exists.
Sex: No sex predilection exists.
Age: AOP affects approximately 70% of neonates aged 34-35 weeks after conception. Although the frequency progressively decreases during their subsequent weeks of life, approximately 30-40% of neonates born prematurely still have AOP at the expected due date. Significant apnea and/or hypoxemic events have been well documented in premature neonates beyond term. The mean time for AOP resolution is approximately 50-52 weeks after conception.
Findings from other recent studies indicate that 6-22% of babies with a very low birth weight have apnea at term, and that 91% of premature neonates have apnea exceeding 12 seconds in duration at the time of hospital discharge. Of these babies, 31% also had bradycardia, and 6.5% required prolonged hospitalization because of the severity of their apnea and bradycardia. These findings show that AOP does not resolve at term in many low-birth-weight infants and that it may be present for some time after hospital discharge.
History:
• Usually, the decrease in PO2 in full-term neonates with apnea is directly proportional to the duration of apnea; it also is significantly greater in obstructive than in central apnea.
• All forms of apnea are difficult to detect visually, although obstructive apnea usually is more obvious to a trained observer.
• Precise apnea diagnosis requires multichannel recordings, which are most commonly used to measure nasal airflow and thoracic impedance, average heart rate, and oxygen saturation.
• Published findings show that even highly trained observers miss more than 50% of AOP episodes.
apnea of prematurity - Physical: The physical examination should include observation of the infant's breathing patterns while he or she is asleep and awake.
• Monitor the baby's cardiac, neurologic, and respiratory status.
• Observe the infant during feeding periods for any signs of breathing difficulty, desaturation, or bradycardia.
• Reflex effects of apnea include characteristic changes in the heart rate, BP, and pulse
pressure. Bradycardia may begin within 1.5-2 seconds of apnea onset. Apneic episodes associated with bradycardia are characterized by heart rate decreases of more than 30% below the baseline rates. This reflex bradycardia is secondary to hypoxic stimulation of the carotid body chemoreceptor or a direct effect of hypoxia on the heart.
apnea of prematurity - Lab Studies:
• A CBC and cultures of blood, urine, and spinal fluid are necessary if a serious bacterial infection is suspected.
• Tests for serum ammonia, urine and serum amino acid, and organic acid levels are useful if a metabolic disorder is suspected.
• Serum electrolyte, calcium, and glucose levels can help in diagnosing a recent stressful condition, metabolic process, or chronic hypoventilation.
• A stool specimen test for botulism helps if the infant with apnea has associated constipation and hypotonia.
apnea of prematurity - Imaging Studies:
• Chest radiography and/or radionuclide milk scanning can help if the child has persistent, yet unexplained, lower airway symptoms.
• Upper airway evaluation, including lateral neck radiography and otolaryngologic evaluation, is useful for cases of fixed or recurrent stridor, as well as cases of unexplained pathologic obstructive apnea.
• Imaging studies of the head are necessary when an intracranial hemorrhage is suspected or when findings include dysmorphic features, abnormal neurologic results, or mental status changes.
• A barium swallow study is useful if the infant has signs of swallowing dysfunction or anatomic anomalies (eg, esophageal web, tracheoesophageal fistula).
• A gastric emptying study and abdominal sonography are useful in patients whose clinical picture includes a generalized GI motility disorder or pyloric stenosis.
apnea of prematurity - Other Tests:
• Perform a continuous multichannel recording to measure the chest-wall movement, nasal and/or oral airflow (or change in air temperature), oxygen saturation, and heart rate trend. (A 2-channel pneumogram that is used to measure only chest-wall excursion and heart rate trend provides insufficient information.) The following results are diagnostic:
o Central apnea - Absence of nasal airflow and wall movement
o Obstructive apnea - Lack of airflow despite chest-wall movement
o Mixed apnea - Combined results of central and obstructive apnea
• If GER is suspected, obtain an intraesophageal pH recording by means of multichannel recording.
• Consider obtaining an electroencephalogram (EEG) in infants in whom apneic seizures are suspected or in whom persistent pathologic central apnea without an identifiable cause is present.
• Obtain an echocardiogram (ECHO), and consult a cardiologist if the history or physical examination results (eg, feeding difficulties, heart murmur, cyanosis) suggest cardiac disease.
• Electrocardiographic (ECG) results are useful in patients with severe unexplained tachycardia or bradycardia. Cardiac conduction abnormalities (eg, prolonged-QT syndrome) are rare but important causes of infant apnea.
• Evaluate unilateral choanal stenosis and choanal atresia by passing a 5-8F feeding tube through both nares. CT scanning is the method of choice for definitive diagnosis.
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