ࡱ> q` bjbjqPqP .x::P;P;P;P;P;P;P;d;<( d;&Sj@. nnnnn RRRRRRR$ThV8RP;nnRP;P;nnR&&&P;nP;nR&R&&ODP;P;1Qn4 f{\i?> P&RR0&S Q&0W}&R0WL1Q1QT0WP;R b|&ThWRR& &Sd;d;d;$NdKd;d;d;d;d;d;P;P;P;P;P;P;   HYPERLINK "http://emedicine.medscape.com"  INCLUDEPICTURE "http://images.medscape.com/pi/global/header/emed/logo-emedicine-print107x27.gif" \* MERGEFORMATINET  Apnea of Prematurity Dharmendra J Nimavat, MD, FAAP, Assistant Professor of Clinical Pediatrics, Department of Pediatrics, Division of Neonatology, Southern Illinois University School of Medicine Michael P Sherman, MD, Professor, Department of Child Health, University of Missouri-Columbia School of Medicine; Director, Fellowship Training Program in Neonatal-Perinatal Medicine, NICU, Columbia Regional Hospital; Professor Emeritus, Department of Pediatrics, University of California, Davis, School of Medicine; Rene L Santin, MD, Consulting Staff, Department of Pediatrics, Division of Neonatology, Primary Care Centers of Eastern Kentucky; Rachel Porat, MD, Director, Neonatal Apnea Monitoring Program, Assistant Director, Division of Neonatology, Albert Einstein Medical Center; Associate Professor, Department of Pediatrics, Thomas Jefferson University Updated: Oct 26, 2009 Introduction Background Overview of the Current State of Knowledge Our understanding of the anatomy, physiology, biochemistry, and molecular biology of neonatal breathing has increased in recent years.1, 2, 3, and 4 For instance, emerging data are elucidating the genes involved in the embryonic development of central respiratory centers and their neural networks.5 The central respiratory generator is essential for fetal breathing movements. It appears early in pregnancy and importantly contributes to pulmonary development.6 In the fetus, breathing is intermittent and occurs during the low-voltage electrocortical state (analogous to rapid eye movement [REM] sleep) and becomes continuous immediately after birth. The regulatory neurologic mechanisms that cause the transition from intermittent fetal breathing to continuous neonatal breathing are incompletely appreciated.7, 8 After birth, apnea of prematurity (AOP) is a major concern for caregivers in intensive care nurseries. The magnitude of this problem resulted in the National Institutes of Child Health and Human Development (NICHD) convening a workshop on apnea of prematurity. Summary Proceedings from the Apnea-of-Prematurity Group have been published.9 The NICHD review group emphasized the following conclusions: No consensus has been reached regarding the definition, diagnosis, or treatment of apnea of prematurity. Systematic research has not been conducted to investigate the value of different interventions for apnea of prematurity. Available technology is not routinely used to document real-time events associated with apnea. The time required to demonstrate an improvement in apnea of prematurity with a specific treatment has not been established. The observational period needed after therapy for apnea of prematurity is unknown, and an appropriate duration of surveillance off therapy is needed to reasonably prevent acute life-threatening events. Important confounding conditions that influence the occurrence of apnea of prematurity are poorly recognized and/or integrated into care. The relationship between gastroesophageal reflux (GER) and apnea of prematurity requires additional investigation because current knowledge suggests an infrequent association. Improved characterization of the effects of apnea of prematurity on neurodevelopment during infancy and childhood is needed. Other confounders associated with brain injury in preterm infants are difficult to separate from apnea of prematurity as meaningful causes of abnormal child development. The NICHD review group also made recommendations about what issues associated with apnea of prematurity that need urgent attention, what research methods might be best for future studies, what outcomes are essential to our understanding of apnea of prematurity, and what ethical principles should govern future investigations of apnea of prematurity. Given this discussion from the NICHD review group, the present article provides state-of-the-art information regarding what is and what is not known about apnea of prematurity. Definitions Apnea and its classification Apnea is defined as the cessation of breathing for more than 20 seconds or apnea or the cessation of breathing for less than 20 seconds if it is accompanied by bradycardia or oxygen (O2) desaturation.10,9 Bradycardia in a premature neonate is considered clinically significant when the heart rate slows by least 30 bpm from the resting heart rate. An O2 saturation level of more than 85% is considered pathologic in this age group, as is a decrease in O2 saturation should it persist for 5 seconds or longer. These definitions represent clinically significant changes in apnea, bradycardia, and O2 saturation changes and 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 (see Media file 1).  INCLUDEPICTURE "http://img.medscape.com/pi/emed/ckb/pediatrics_cardiac/1331339-1331345-974971-975105.jpg" \* MERGEFORMATINET  Central apnea is defined as the cessation of both airflow and respiratory effort. ECG = electrocardiogram; HR = heart rate; THO = thoracic impedance; FLOW = air flow; ACT = ; SpO2 = peripheral oxygen saturation; STAGE = sleep stage. Obstructive apnea is the cessation of airflow in the presence of continued respiratory effort. Mixed apnea contains elements of both central and obstructive apnea (see Media file 2), either within the same apneic pause or at different times during a period of respiratory recording.  INCLUDEPICTURE "http://img.medscape.com/pi/emed/ckb/pediatrics_cardiac/973235-974971-1738.jpg" \* MERGEFORMATINET  Polysomnogram. Mixed apnea contains elements of both central and obstructive apnea. ECG = electrocardiogram; HR = heart rate (bpm); THO = thoracic movement; FLOW = flow from the nose and mouth; ACT = gross body movement; SpO2 = peripheral oxygen saturation (%); STAGE = sleep stage, where AT = active sleep. 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 and AOI coincide, though further studies are needed to determine their exact relationship. Periodic breathing Periodic breathing is defined as periods of regular respiration for as long as 20 seconds followed by apneic periods of 10 seconds or less that occur at least 3 times in succession (see Media file 3).  INCLUDEPICTURE "http://img.medscape.com/pi/emed/ckb/pediatrics_cardiac/973235-974971-1739.jpg" \* MERGEFORMATINET  Polysomnogram. Periodic breathing 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. ECG = electrocardiogram; HR = heart rate (bpm); THO = thoracic movement; FLOW = flow from the nose and mouth; ACT = gross body movement. Periodic breathing may be observed for 2-6% of the breathing time in healthy term neonates and as much as 25% of the breathing time in preterm neonates. The occurrence of periodic breathing is directly proportional to the degree of prematurity. Kelly and coworkers observed periodic breathing in 78% of neonates examined at 0-2 weeks of age.11 The incidence substantially declined to 29% at the postconceptual ages of 39-52 weeks. Periodic breathing typically does not occur in neonates during their first 2 days of life. Periodic breathing most frequently occurs during active sleep, but it can also happen when neonates are awake or quietly sleeping. This pattern, commonly observed in patients at high altitudes, is eliminated with supplemental oxygenation and/or with the use of continuous positive airway pressure (CPAP). Because the prognosis is excellent and because the infant is not compromised, no treatment is usually required. Pathophysiology Central respiratory regulation Immaturity and/or depression of the central respiratory drive to the muscles of respiration have been accepted as key factors in the pathogenesis of apnea of prematurity.1 Vulnerability of the ventral surface of the medulla and adjacent areas in the brainstem to inhibitory mechanisms is the likely explanation for why apneic episodes occur in prematurely born infants. This vulnerability involves diverse clinicopathologic events.12,4 Inhibitory events that affect the central respiratory generator and initiate apnea include hypoxia, hyperthermia and adenosine secretion.13 Studies of preterm infants and in animals (especially genetically altered mice) have enhanced our understanding of the molecular and biochemical events leading to maturation of the central respiratory generator in preterm infants.2,3,14,15 Using noninvasive techniques, Henderson-Smart and coworkers documented that brainstem conduction times of auditory-evoked responses were longer in infants with apnea than in matched premature infants without apnea.16 This study elucidated apnea in preterm infants by indirectly showing that infants with apnea had greater-than-expected immaturity of brainstem function, which was based on postconceptional age. This finding supports the concept than an immature brainstem eventually develops control of breathing as dendritic spines and synaptic connections mature. An observation that emphasizes the importance of the central respiratory generator is the finding of increased apnea among preterm infants with bilirubin-encephalopathy diagnosed by using abnormal auditory brainstem-evoked responses.17 The absence of respiratory muscle activity during central apnea unequivocally implicates depression of respiratory center output. In support of this concept, Gauda and associates (1989) documented reduced electromyographic activity in the diaphragm during spontaneous obstructed inspiratory efforts.18 Such efforts characterize combined central and obstructive apnea.19 Therefore, episodes of both central and mixed apneic share an element of decreased respiratory center output to the respiratory muscles. Sleep state and apnea Apnea during infancy occurs most frequently during active or REM sleep.20,21 Apnea occurs relatively infrequently during quiet sleep, when respiration is characteristically regular, with little breath-to-breath variation in tidal volume and respiratory rate. However, periodic breathing may predominantly occur during non-REM sleep. During active sleep, respiration is mostly paradoxical due to spinal motoneural inhibition of the activity of intercostal muscles.22 In extremely preterm infants, the paucity of quiet sleep, together with an extremely compliant rib cage, makes paradoxical chest-wall movements almost a constant phenomenon. Paradoxical chest movement may predispose the baby to apnea by decreasing functional residual capacity (FRC) and limiting oxygenation.23 Chemoreceptors and mechanoreceptors Complex relationships exist between respiratory control; several sites of central chemosensitivity to carbon dioxide (CO2) during sleep; and various neuromechanical factors originating in the lungs, chest wall, and upper airway that modify respiratory function during sleep.24 Responses of chemoreceptors in preterm and term neonates were recently reviewed.25,26,27 The response to elevated CO2 concentrations was blunted in prematurely born infants. This diminished response may partly be due to decreased central chemosensitivity or mechanical factors that prevent an adequate ventilatory response.28,29 The slope of the response curve for CO2 is decreased for preterm infants who have apnea.30 However, a cause-and-effect relationship between decreased CO2 responsiveness and apnea of prematurity has not been clearly established. Administration of CO2 ameliorates periodic breathing, but inhalation of CO2 is not a therapeutic option for human infants. For many years, scientists have known that preterm infants respond to a decrease in inspired O2 concentration with a transient increase in ventilatory response, followed by return to baseline or even depression of ventilation.31 This response to low O2 in infants appears to result from initial stimulation of peripheral chemoreceptors then overriding depression of the respiratory center as a result of hypoxemia.32 Consistent with these findings is the observation that a progressive decrease in inspired O2 concentrations causes a significant flattening of CO2 responsiveness in preterm infants.33 This unstable response to low inspired O2 levels may play an important role in the origin of neonatal apnea. It offers a physiologic rationale for the decrease in incidence of apnea observed when a slightly increased concentration of inspired O2 is administered to infants with apnea.34 The Hering-Breuer reflex also plays an important role in modulating respiratory timing in human neonates. Pulmonary stretch receptors send an afferent neural input to brain and mediate the Hering-Breuer reflex by means of the vagus nerve. Thereafter, they inhibit inspiration, prolong expiration, or both, while increasing lung volume.23 Active shortening of expiratory duration with decreased lung volume may provide a breathing strategy for preserving FRC in a neonate with a highly compliant chest wall. Upper airway obstruction substantially contributes to apneic episodes in preterm infants, and upper airway muscles show preferential reflex activation in response to airway obstruction in infants.35 Gerhardt and Bancalari compared the ability of preterm infants with and those without apnea to respond to end-expiratory airway occlusion.36,30 Prolongation of the occluded inspiratory effort was significantly prolonged in the group without apnea. This finding suggested that this group had a relatively mature respiratory reflex response that improved their ability to respond to airway obstruction. In premature infants, complex changes in pulmonary mechanics and ventilatory timing accompany apnea.37 Before apnea occurs, total pulmonary resistance may increase in association with a decrease in tidal volume and prolongation of the expiratory time. Such changes have been noted before episodes of mixed, obstructive, and central apnea. In 1982, Waggener and coworkers showed that a diminution in respiratory drive precedes apnea, a finding reminiscent of the cyclic alterations in respiratory drive.38 After apnea resolves and respiration resumes, the respiratory drive in premature infants initially increases, possibly because of a cumulative effect of hypoxia and hypercapnia. Total pulmonary and supraglottic resistance also increases, perhaps in response to a decrease in lung volume and collapse of the upper airway when respiratory drive declines during the apnea. Of note, within 2 or 3 breaths after apnea, pulmonary resistance and respiratory drive is restored to normal pre-apnea values in premature infants. Therefore, the neural systems that restore respiratory homeostasis appear to be capable of mounting an adequate response, even in premature infants with apnea. Upper airway instability and muscles of the chest wall Premature infants have pharyngeal or laryngeal obstruction during spontaneous apnea. Thach (1983) proposed a model in which the negative luminal pressures generated during inspiration in the upper airway predispose a compliant pharynx to collapse.39 Many muscles of the upper airway, especially the genioglossus muscles, have been widely implicated in mixed and obstructive apnea affecting both infants and adults. Carlo, Martin, and Difiore compared the activity of the genioglossus muscles with that of the diaphragm in response to hypercapnic stimulation.40 In preterm infants, genioglossus activation was delayed for about one minute after CO2 rebreathing was begun, and it occurred only after a CO2 threshold of approximately 45 mm Hg was reached. In neonates inspiratory time is often modestly prolonged when end-expiratory airway occlusion prevents lung inflation. As indicated earlier, this effect is a manifestation of the Hering-Breuer reflex. Studies in animals demonstrated that this vagally mediated inhibition of normal lung inflation has more influence on the upper airway muscles than on the diaphragm.41 Upper airway reflexes The upper airway contains many sensory nerve endings that may respond to various chemical and mechanical stimuli. Sensory input from these upper airway receptors travels to the CNS by means of cranial nerves V, VI, IX, X, XI, and XII. They may strongly affect respiratory rate and rhythm, heart rate, and vascular resistance.42 The chemoreceptor drive may augment the ability of the upper airway muscles to respond to increasing negative pressure, whereas input from pulmonary stretch receptors inhibits it.43 Swallowing during the respiratory pause is unique to apnea and does not occur during periodic breathing.44 Effects of adenosine Adenosine and its analogs cause respiratory depression.45 Adenosine antagonism is proposed as a mechanism to explain the therapeutic effect of aminophylline.46 Gastroesophageal reflux GER and apnea are common in preterm infants. Because they often coexist, a lively and ongoing debate persists among healthcare professionals about the role of GER in apnea of prematurity. An extensive literature review was undertaken to justify arguments about the role of GER in apnea of prematurity. Monitoring studies demonstrated that, when a relationship between reflux and apnea is observed, apnea may precede rather than follow reflux.47,48 During an apneic episode, loss of respiratory neural output may be accompanied by a decrease in lower esophageal tone, and GER occurs. This phenomenon is supported by data from a newborn piglet model, which showed that hypoxia and apnea were accompanied by a reduction in lower esophageal sphincter pressure, which was a predisposing factor for GER.49 GER and apnea are also discussed in Differentials and in Special Concerns. Frequency United States Although not always apparent, apnea of prematurity is the most common problem in premature neonates.9 Approximately 70% of babies born before 34 weeks of gestation have clinically significant apnea, bradycardia, or O2 desaturation during their hospital stay. The more immature the infant, the higher his or her risk of apnea of prematurity. Apnea may occur during the postnatal period in 25% of neonates who weighed less than 2500 g at birth and in 84% of neonates who weigh less than 1000 g. Carlo and Barrington showed that apnea may begin on the first day of life in neonates without respiratory distress syndrome.50,51 However, apnea of prematurity is always a diagnosis of exclusion. Many diseases manifest with apnea on the day of birth; examples are intrapartum magnesium exposure, systemic infections or the fetal inflammatory response syndrome, pneumonia, intracranial pathology, seizures, hypoglycemia, and other metabolic disturbances. Approximately 50% or more of surviving infants who weighed less than 1500 g at birth have episodes of apnea that must be managed with pharmacologic intervention or ventilatory support. Mixed apnea accounts for about 50% of all cases of apnea in premature neonates; about 40% are central apneas, and 10% are obstructive apneas.52 These percentages vary in different reports. In 50% of all apneic episodes, an obstructive component precedes or follows central apnea, which leads to mixed apnea. International To the authors' knowledge, no investigators have compared the incidence of apnea of prematurity in the United States with those of other countries. Mortality/Morbidity Butcher-Puech and coworkers found that infants in whom obstructive apnea exceeded 20 seconds had an increased incidence of intraventricular hemorrhage, hydrocephalus, prolonged mechanical ventilation, and abnormal neurologic development after their first year of life.53 In 1985, Perlman and Volpe described a decrease in the cerebral blood flow velocity that accompanies severe bradycardia (heart rate <80 bpm).54 Infants with clinically significant apnea of prematurity do not perform as well as prematurely born infants without recurrent apneas during neurodevelopmental follow-up testing.55,56 Race The authors know of no systematic, prospective clinical study that has been conducted to evaluate the role of a person's race or ethnic background on the incidence of apnea of prematurity. Sex To the authors' awareness, no systematic, prospective clinical study has been performed to evaluate the role of a person's sex on the incidence of apnea of prematurity. Age A young gestational age at birth is associated with an increased incidence of apnea of prematurity. The age at which apnea of prematurity resolves depends on several factors. The mean time for severe apnea of prematurity to resolve is approximately 43 weeks after conception, but a prolonged duration of risk is not uncommon.10 In one report, about 6-22% of babies with a very low birth weight had apnea at term.57 Approximately 91% of premature neonates had apnea of longer than 12 seconds 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 apnea of prematurity does not resolve at term in many low birth weight infants and that it may persist for some time after hospital discharge. Clinical History Initial identification and assessment of apnea The bedside caregiversnamely, the nurse in the neonatal intensive care unit (NICU) the respiratory care practitioneridentify the problem for the physician. Apnea should be distinguished from periodic breathing and documented. Use of a cardiorespiratory monitor is essential for identifying apnea of prematurity (AOP) and for monitoring the patient's blood pressure. Events associated with apnea, such as bradycardia and cyanosis, must be quantified. For bradycardia, the magnitude of reduction in heart rate from baseline and the duration of the event should be recorded. The presence and duration of central cyanosis should also be noted. Pulse oximetry may be helpful for measuring the severity and duration of central O2 desaturation. Caregivers should be aware of the problems associated with the use of pulse oximetry to evaluate O2 saturation.58 When apnea is observed, its duration must be established. Cardiorespiratory monitors can be used to quantify the duration. Caregivers should attempt to define the type and severity of the patient's apnea. The type of apnea is identified as central, obstructive, or mixed. A nasal thermistor may be needed in conjunction with pneumography to differentiate the type of apnea. Classification of the severity of apnea Criteria to classify the severity of apnea have not been well developed in clinical studies. The University of Washington published indications for different treatments based on the severity of apnea of prematurity.59 This classification for apnea of prematurity uses the terms spontaneous, mild, moderate, or severe. A spontaneous event might be defined by apnea with minimal physiologic changes, an event of brief duration, one associated with self-recovery, or an event only occurring once or twice in 24 hours. Mild or moderate events involve apnea, bradycardia, and/or O2 desaturation of intermediate magnitude. These events require therapeutic interventions less rigorous than those needed for severe episodes. A severe event entails prolonged apnea associated with clinically significant and persistent bradycardia, as well as O2 desaturation (ie, central cyanosis). A severe event requires vigorous stimulation, administration of an increased concentration of inspired O2, and/or assisted ventilation (eg, bag-mask ventilation). Clinical centers must develop the classification system they wish to use to measure the severity of apnea. Factors often used to judge the need for future interventions include these: Severity of the apnea Number of events per day Magnitude of the intervention required to alleviate the event The therapeutic approach used in most NICUs involves a progression from tactile stimulation to methylxanthine therapy and then some form of assisted breathing (eg, nasal continuous airway pressure or assisted ventilation). Exclusion of other causes of apnea Before a diagnosis of apnea of prematurity is made, other causes of apnea in neonates must be excluded (see Differentials). All forms of apnea may be difficult to detect visually, although obstructive apnea is usually most obvious to a trained observer. Cardiorespiratory monitoring and pulse oximetry have improved bedside detection of apnea of prematurity.60 Caregivers should familiarize themselves with the advantages and disadvantages of cardiorespiratory monitoring and pulse oximetry in neonates. Published findings show that even highly trained observers miss more than 50% of apnea of prematurity episodes. Precise diagnosis of apnea of prematurity requires multichannel recordings, which are most commonly measurements of nasal airflow, thoracic impedance, heart rate, and O2 saturation. Expanded testing may include electroencephalography and/or use of an esophageal pH probe with a high thoracic Clark electrode. Hydrochloric acid may be added to the feedings to increase the gastric concentration of hydrogen ions. Physical Physical examination should include observation of the infant's breathing patterns while he or she is asleep and awake. The prone or supine sleeping positions and other lying postures may be important during this clinical observation. Important to the assessment of neonatal apnea is the identification of airway abnormalities (eg, choanal obstruction, anomalies of the palate, jaw deformities, neck masses) and conditions in distant organs that influence breathing (eg, brain hemorrhages, seizures, pulmonary disorders, congenital heart disease). Findings in the head and neck and other obvious major and minor anomalies identified may suggest chromosomal abnormalities or a malformation syndrome. Appropriate work-up must then follow. Physical examination includes the elements described below: Monitor the baby's cardiac, neurologic, and respiratory status. Observe the infant for any signs of breathing difficulty, desaturation, or bradycardia during feeding. Reflex effects of apnea include characteristic changes in heart rate, blood pressure, and pulse pressure. Bradycardia may begin within 1.5-2 seconds of the onset of apnea. Apneic episodes associated with bradycardia are characterized by decreases in heart rate of more than 30% below baseline rates. This reflex bradycardia is secondary to hypoxic stimulation of the carotid body chemoreceptor or a direct effect of hypoxia on the heart. Transient bradycardias also occur relatively often in very low birth weight infants who also have apnea of prematurity.61 These events are not associated with apnea, but they are presumed to be mediated by an increase in vagal tone. Pulse oximetry may reveal clinically significant desaturation. However, pulse oximeters typically have a delay in recording the event. Causes The physiology related to apnea of prematurity is reviewed in Pathophysiology. Aspects of causation are briefly reemphasized here. A premature neonate in whom all other causes of apnea have been excluded may be considered to have apnea of prematurity. Although the etiology of apnea of prematurity is not fully understood, several mechanisms have been proposed to explain this condition, including those described below. Apnea of prematurity is the clinical phenomenon associated with incompletely organized and interconnected respiratory neurons in the brainstem and their response to a multitude of afferent stimuli. Therefore, the abnormal control of breathing seen in apnea of prematurity represents neuronal immaturity of the brain. (For an excellent review of this topic, see the article by Darnall et al.1 ) In a premature neonate, protective respiratory reflex activity is decreased, and Hering-Breuer reflex activity is increased. Dopaminergic receptors may have a role in inhibiting the responses of peripheral chemoreceptor and hypoxia-elicited central neural mechanisms. Evidence from studies of neonatal animals indicates that endogenous endorphin production may depress the central respiratory drive. Although endogenous opiates may modulate the ventilatory response to hypoxia in newborn animals, a competitive opiate receptor antagonist (naloxone) has no therapeutic role in apnea of prematurity. Negative luminal pressures are generated during inspiration, and the compliant pharynx of the premature neonate is predisposed to collapse. Failure of genioglossus activation is most widely implicated in mixed and obstructive apnea among infants and adults. The ability of medullary chemoreceptors to sense elevated CO2 levels is impaired. Therefore, an absent, small, or delayed response of the upper airway muscles to hypercapnia might cause upper airway instability when a linear increase in chest-wall activity also occurs. This impairment may predispose the infant to obstructed inspiration after a period of central apnea. Another important factor to consider is the excitation of chemoreceptors in the larynx due to acid reflux. Laryngeal receptors send afferent fibers to the medulla and can elicit apnea when stimulated. Swallowing during a respiratory pause is unique to apnea and does not occur during periodic breathing. Accumulation of saliva in the pharynx could hypothetically prolong apnea by means of a chemoreflex mechanism. Some practicing neonatologists believe that gastroesophageal reflux (GER) is associated with recurrent apnea and have, therefore, treated preterm neonates with antacid and/or antireflux drugs. However, this assumption has been vigorously challenged.9 Booth suggested that apneic episodes were reduced when esophagitis resolved because apnea clinically improved 1 or 2 days after the start of antireflux therapy. Therefore, neonatologists have treated xanthine-resistant apnea with H2 blockers, metoclopramide, thickened formula, and/or upright positioning during feeding. No controlled trials have demonstrated that antireflux drugs are effective in preventing apnea. Findings from several studies have not demonstrated a relationship between episodes of apnea and episodes of acid reflux into the esophagus (see Pathophysiology and Differentials). Menon, Schefft, and Thach observed that regurgitation of formula into the pharynx after feeding was associated with an increased incidence of apnea in premature infants.62 As stated above, gastric fluids can possibly activate laryngeal chemoreflexes, leading to apnea. Although well-designed, controlled clinical trials are few, scientists often say that aminophylline exacerbates reflux in infants with apnea. The relationship of GER to methylxanthines is based on the literature about asthma, and limited studies in neonatal only suggest its occurrence.63 Some authors have not related the use of methylxanthine to severe GER disease.64 Differential Diagnoses Anemia of Prematurity Neonatal Sepsis Respiratory Failure Respiratory Syncytial Virus Infection Other Problems to Be Considered Apnea of prematurity (AOP) is a diagnosis of exclusion. For many diseases in preterm infants, apnea is a presenting symptom. The causes of these diseases are different when the differential diagnosis occurs shortly after birth compared with later in the patient's hospital stay. Other etiologies must be sought before drug and/or ventilatory therapies for apnea of prematurity are started. Conditions Associated with Apnea Shortly after birth, apnea can be a manifestation of several types of conditions: Respiratory distress syndrome and other pulmonary conditions Infections (eg, congenital pneumonia, bacteremia, meningitis, fetal or neonatal inflammatory response syndrome) Hypoglycemia and other metabolic diseases CNS pathology (eg, trauma, intracranial hemorrhage, anoxia and/or ischemia, stroke) The aforementioned brain insults may be noticed because patients may have seizures and/or associated apnea.65,54 Some of the diseases cited above also occur relatively late during the hospitalization of prematurely born infants, but the signs and symptoms may or may not include apnea. Intraventricular hemorrhage and posthemorrhagic hydrocephalus without seizures increases the frequency of apnea in preterm infants.53,66 Other Conditions Associated with Apnea in Preterm Infants During Hospitalization Other conditions associated with apnea in preterm infants during their hospitalization are summarized below. Nosocomial bacterial or fungal infection Apnea, bradycardia, and desaturations are presenting symptoms of nosocomial infections caused by bacteria and fungi or viral agents.67,68 In a study of 9 infants in an NICU who had respiratory syncytial viral infection, 8 had apnea as a manifestation of disease.69 Apnea is also common in preterm infants with Ureaplasma urealyticum infection.70 Necrotizing enterocolitis In addition, apnea is one of several signs and symptoms associated with the onset of necrotizing enterocolitis.71 Exposure to magnesium The administration of magnesium to prevent seizures in preeclampsia and tocolysis of preterm labor has been associated with hypoventilation, apnea, and other adverse effects in preterm infants.72 Hypermagnesemia during parenteral nutrition has also been a cause of apnea.73 Anemia Disagreement exists regarding the role of clinically significant anemia in the development of apnea among convalescing preterm infants. Westkamp and colleagues reported that blood transfusions lowered heart and respiratory rates but had little effect on apnea of prematurity.74 Bell and associates conversely found that liberal versus restrictive blood transfusion significantly reduced apnea.75 The recent interest in the adverse neurodevelopmental outcomes observed in preterm infants with anemia and low iron status emphasizes neonatology-related awareness of the problem.76 Surgery Postoperative apnea occurs in preterm infants, particularly those whose intraoperative pain relief involved general anesthesia.77,78 Additional research is required to determine whether spinal anesthesia, different analgesic agents, or caffeine can mitigate morbidity associated with apnea after surgery in prematurely born infants.79,80 Immunization Apnea transiently increases or recurs in hospitalized preterm infants after immunization. The increase in apnea has been attributed to the whole-cell pertussis component.81 Investigators have observed reduced morbidity with newer vaccines that contain acellular pertussis.82,83 Some recent reports still identified clinically significant apnea and other adverse events.84,85 Gastroesophageal reflux As stated earlier, controversy exists regarding the role of gastroesophageal reflux (GER) as a causative factor in apnea of prematurity.9 One perspective is that the 2 conditions are related.63,86 Laryngeal edema identified during fiberoptic laryngeal endoscopy has been associated with GER, and antireflux surgery has dramatically reduced apnea in preterm infants at highest risk.87,88,89 Past and recent research failed to reveal a temporal relationship between GER and apnea of prematurity.47,90,91,92,48 Therefore, the NICHD Review Group on Apnea of Prematurity has called for additional investigations with rigorous research designs.9 Skin-to-skin contact, or kangaroo care Skin-to-skin contact, or kangaroo care, for preterm infants has been associated with an increased occurrence of apnea, bradycardia, and desaturation; this appears to be unrelated to hyperthermia.93,94 The observation suggests that obstructive events may occur during skin-to-skin contact. These findings call attention to the importance of environmental hyperthermia as a cause of apnea in preterm infants.95,96 Recent investigators found no adverse events during kangaroo care.97 The disparity among the reported studies may be related to the specific practice of skin-to-skin care in a particular NICU or the validity of monitoring during skin-to-skin contact.98 Workup Laboratory Studies A CBC count and cultures of blood, urine, and spinal fluid are necessary if a serious bacterial or fungal infection is suspected in patients with apnea of prematurity (AOP). Appropriate viral cultures or collection of body fluid for polymerase chain reaction (PCR) analyses are performed if a viral pathogen was suspected. A C-reactive protein level measured at 36-48 hours after birth may be useful for excluding infection (see Maternal Chorioamnionitis). Tests for ammonia, amino acid profiles in blood or urine, and organic acid levels in blood and urine are essential if a metabolic disorder is suspected. Testing of pyruvate and lactate concentrations in the blood and cerebrospinal fluid (CSF) may be diagnostically helpful when inborn errors of metabolism are among the differential diagnosis. Ketones in the urine may indicate organic acidemia. Serum electrolyte, calcium, magnesium, and glucose levels can be useful for diagnosing a recent stressful condition, a metabolic process, or chronic hypoventilation. Analysis of the stool for different toxins related to botulism may reveal a cause in an infant with apnea, constipation, clinically significant hypotonia, difficulty swallowing or crying, or absent eye movements.99 Imaging Studies Chest radiography and/or a nuclear medicine milk scanning can be helpful if the child has persistent but unexplained lower airway symptoms (eg, wheezing and/or repetitive regurgitation after feeding, rumination).100 In cases of airway obstruction, stridor, or unexplained pathologic obstructive apnea, helpful upper airway evaluations include lateral neck radiography, head and neck 3-dimensional tomography, and otolaryngologic evaluation (eg, fiberoptic assessment of the larynx through the nose during spontaneous breathing).101 Imaging studies of intracranial pathology are necessary when hemorrhage is suspected or when findings include dysmorphic facial and somatic features, abnormal neurologic results, disordered hair whorls, and/or mental status changes. A barium swallow study is useful if the infant has signs of swallowing dysfunction or anatomic anomalies (eg, an 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. Other Tests Obtain a polysomnographic, or continuous multichannel, recording to measure the chest-wall movement, nasal and/or oral airflow (or change in air temperature), O2 saturation, and heart rate trend. A 2-channel pneumogram that is used to measure only chest-wall excursion and trends in heart rate provides insufficient information. The following results are diagnostic: Central apnea - Absence of nasal airflow and wall movement Obstructive apnea - Lack of airflow despite chest-wall movement Mixed apnea - Combined results of central and obstructive apnea If gastroesophageal reflux (GER) is suspected, note the intraesophageal pH as part of the multichannel recording. Consider obtaining an electroencephalogram (EEG) in infants who have suspected apneic seizures or who have persistent pathologic central apnea without an identifiable cause. Obtain an echocardiogram and consult a cardiologist if the patient's history or physical findings (eg, feeding difficulties, heart murmur, cyanosis) suggest cardiac disease. ECG results are useful in patients with severe unexplained tachycardia or bradycardia. Abnormalities in cardiac conduction (eg, prolonged-QT syndrome) are infrequent but important causes of apnea during infancy. Evaluate patients for unilateral choanal stenosis and choanal atresia by passing a small-diameter feeding tube through both nares. Three-dimensional tomography is probably the method of choice for definitively diagnosing upper airway malformations. Procedures Several studies may reveal diagnostic findings in selected infants. These include fiberoptic examination of the larynx through the nose during spontaneous breathing, direct laryngoscopy, and bronchoscopy (which is usually performed with the patient under anesthesia). Emergency or scheduled tracheostomy may be used to managesevere airway obstruction caused by a number of conditions. Tracheostomy might occur after the airway is stabilized by using endotracheal intubation. Jaw-distraction surgery was recently used to avoid tracheostomy in neonatal conditions (eg, Robin sequence) that involve severe micrognathia as a component of malformation.102,103 Treatment Medical Care Goal of medical therapy The principal goals of treating apnea of prematurity (AOP) are to address its cause and to provide appropriate medical management. For example, bacterial sepsis that causes apnea is treated with antibiotics and other supportive therapies, whereas seizures require anticonvulsants. The use of assisted ventilation to manage severe apnea, bradycardia, and O2 desaturation can be life saving, and assisted ventilation and O2 may be required to prevent injury to the CNS. The primary disease process must be identified and treated. When all causes of apnea other than prematurity are excluded during the diagnostic work-up, apnea of prematurity is the presumptive etiology. Caregivers must decide which intervention is appropriate given the severity of the patient's apnea, bradycardia, and O2 desaturation. For example, an infant who has an inadequate response to tactile stimulation and O2 administration and who requires airway suctioning and bag-mask ventilation to recover suggests a serious problem. A useful strategy is to have a protocol that defines escalating treatments for apnea of prematurity. Depending on the frequency and the severity of apnea, bradycardia, and O2 desaturation, common treatments include stimulation (usually tactile), methylxanthine, or assisted ventilation (eg, nasal continuous positive airway pressure [CPAP], mechanical ventilation).104 Pantalitschka et al compared 4 modes of nasal respiratory support for apnea of prematurity in very low birthweight infants: intermittent positive pressure ventilation (IPPV) via a conventional ventilator or a variable flow device and CPAP via a variable flow device or a constant flow underwater bubble system.105 In their randomized controlled trial with a crossover design, episodes of bradycardia or desaturation occurred at a rate of 6.7 per hour with the conventional ventilator in IPPV mode and at a rate of 2.8 and 4.4 per hour with the variable flow device in CPAP and IPPV mode, respectively (P<0.03 for both compared with IPPV/conventional ventilator). Pantalitschka et al concluded that a variable flow nasal CPAP may be more effective than a conventional ventilator in nasal IPPV mode for treating apnea of prematurity. Stimulation Tactile stimulation is usually sufficient to terminate an isolated apneic event caused by central apnea. Stimulation akin to that used during neonatal resuscitation (eg, a gentle tap to the sole of the foot or rubbing the back) is often enough to terminate a central apnea. However, other measures may be required to treat an obstructive event or an episode of airway obstruction followed by central apnea. If the upper airway is obstructed, repositioning the patient's head and neck or gently elevating the infant's jaw may alleviate the occlusion. Use of a high-flow nasal cannula may open the airway enough to reduce obstructive apnea. As an alternative, high-flow oxygenation through a nasal cannula may be an agonist for receptors in the airway. Nasal irritation due to the cannula may prevent central apnea by causing arousal. Additional research is needed to ascertain the usefulness of high-flow nasal cannulas for treating apnea of prematurity. Administration of O2 Supplemental oxygenation or bag-mask ventilation is indicated in infants with signs of bradycardia or desaturation. Medical treatment is indicated when apneic episodes number 6-10 or more per day; when the infant does not respond to tactile stimulation; or when an event requires O2 and/or bag-mask ventilation to terminate apnea, bradycardia, and/or desaturation. Avoid hyperoxia, which may increase the risk of retinopathy of prematurity (ROP). Use of CPAP CPAP has been used to treat apnea in preterm neonates, and it is indicated when the infant continues to have apneic episodes despite achieving a therapeutic serum level of methylxanthine. CPAP is delivered with nasal prongs, a nasal mask, or a face mask with 3-6 cm of water pressure. CPAP effectively treats mixed and obstructive apnea, but it has little or no effect on central apnea. This limitation suggests that CPAP may reduce the frequency of apnea by means of several mechanisms, including stabilization of the partial pressure of O2 (PaO2) by increasing the functional residual capacity (FRC), by altering the influence of stretch receptors on respiratory timing, or by splinting the upper airway in an open position. Medication Methylxanthines Methylxanthines may help reduce the incidence of events in a neonate with central apnea, though apnea in 15-20% of infants does not respond to methylxanthines. Questions have been raised regarding short- and long-term adverse effects in preterm infants.106 The relationship of methylxanthine therapy to neurodevelopmental outcomes over time is especially of concern. For this reason, a clinical trial related to the safety of caffeine in preterm infants with apnea of prematurity (AOP) is in progress.107 For the purpose of this review, pharmacotherapy is based on the 2006 NeoFax.104 This is the source for information regarding the administration, adverse effects, and interactions of methylxanthines (eg, drug and solution compatibility). Caffeine Caffeine is the preferred drug for treating apnea of prematurity.80 Caffeine is also the most acceptable prophylactic agent to facilitate successful extubation in preterm infants.108 Caffeine therapy may reduce the rate of bronchopulmonary dysplasia in very low-birth-weight infants.109 In addition, caffeine has a therapeutic margin wider than that of other methylxanthines, such as theophylline. Therefore, an overdose is less likely to occur with caffeine than with other drugs in its class. Aminophylline Aminophylline is the alternative methylxanthine. Aminophylline may be preferred when the physician wants to enhance contractility in the thoracic musculature or if the infant might benefit from the bronchodilator properties of aminophylline.110,111 This latter effect may be desired in infants with bronchopulmonary dysplasia. One concern is that aminophylline may decrease cerebral blood flow.112,113,114,115,116 Early reports in the literature also indicate a concern about the role that aminophylline may play in the occurrence or severity of necrotizing enterocolitis.117,118,119 Doxapram Doxapram is excluded as a therapy for apnea of prematurity because it is associated with reduced cerebral blood flow.120,121 Use of doxapram was not strongly recommended in a Cochrane Review.122 Doxapram should be reserved for infants in whom appropriate methylxanthine therapy and continuous positive airway pressure (CPAP) fail to control severe apneic events. If the caregiver wishes to use this agent, they should consult other resources regarding its administration. Home Monitoring Home monitoring after discharge is always necessary for infants whose apneic episodes continue despite the administration of methylxanthine. Infants undergoing methylxanthine therapy should rarely be sent home without a monitor because apnea may recur when they outgrow their therapeutic level. Some families cannot manage monitoring in the home. In these cases, caffeine may be the only possible therapy. For more information about follow-up care, see Follow-up. Methylxanthines Aminophylline appears to stimulate skeletal and diaphragmatic muscle contraction, increase the sensitivity of the ventilatory center to CO2, and stimulate the central respiratory drive. Aminophylline, theophylline, and caffeine act as nonspecific inhibitors of adenosine A1 and adenosine A2a receptors.106 It is this last effect that raises concerns about the safety of methylxanthine therapy in preterm infants. Aminophylline (Aminophyllin) Indications include AOP (eg, apnea after extubation from assisted ventilation, apnea after general anesthesia, apnea during use of prostaglandin E1 to treat ductal-dependent heart defects). Stimulates central respiratory drive and peripheral chemoreceptor activity; may increase diaphragmatic contractility. Aminophylline salt is 78.9% theophylline; theophylline PO is 80% bioavailable. May need to adjust dose when changing from IV aminophylline to PO theophylline. In neonates, aminophylline significantly (30-80%) interconverted to caffeine. IV and PO forms effective in about 80-85% of infants with central apnea. Dosing Adult Pediatric Based on aminophylline (ie, not theophylline equivalent) Loading dose: 4-8 mg/kg PO or IV over 30 min Maintenance dose: 1.5-3 mg/kg/dose PO q8-12h or slow IV bolus q8-12h; start 8-12 h after loading dose Therapeutic theophylline serum concentration (trough) for AOP is 7-12 mcg/mL; target theophylline serum concentration is 10-20 mcg/mL for bronchospasm in older infants (ie, some infants with bronchopulmonary dysplasia) Interactions Aminoglutethimide, barbiturates, carbamazepine, ketoconazole, loop diuretics, charcoal, hydantoins, phenobarbital, phenytoin, rifampin, isoniazid, and sympathomimetics may decrease effects of theophylline; allopurinol, beta-blockers, ciprofloxacin, corticosteroids, disulfiram, quinolones, thyroid hormones, ephedrine, carbamazepine, cimetidine, erythromycin, macrolides, propranolol, and interferon may increase effects of theophylline May be associated with renal calcifications when used concurrently with furosemide and/or dexamethasone IV incompatible with amiodarone, cefotaxime, ceftriaxone, clindamycin, dobutamine, epinephrine, hydralazine, insulin, isoproterenol, methadone, methylprednisolone, penicillin G, and phenytoin Solution compatible with 5% or 10% dextrose in water and normal saline Terminal injection site compatible with dextrose and amino acid solutions, lipid emulsions, acyclovir, ampicillin, amikacin, aztreonam, calcium gluconate, cefazolin, ceftazidime, dexamethasone, dopamine, enalaprilat, erythromycin lactobionate, famotidine, fluconazole, furosemide, heparin, hydrocortisone succinate, isoproterenol, lidocaine, methicillin, meropenem, metronidazole, midazolam, morphine, nafcillin, nitroglycerin, nitroprusside, pancuronium bromide, pentobarbital, phenobarbital, piperacillin, potassium chloride, prostaglandin E1, ranitidine, sodium bicarbonate, ticarcillin/clavulanate, tobramycin, vancomycin, and vecuronium Contraindications Documented hypersensitivity; uncontrolled arrhythmias; peptic ulcers; hyperthyroidism; uncontrolled seizure disorders Precautions Pregnancy C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus Precautions Emphasize slow IV infusion because changes in cerebral blood flow may occur Caution with peptic ulcers, hypertension, tachyarrhythmias, hyperthyroidism, and compromised cardiac function; increased risk of toxicity in pulmonary edema or liver dysfunction because of reduced clearance; periodically monitor heart rate and blood glucose; consider withholding next dose if heart rate >180 bpm; may produce GI irritation, hyperglycemia, CNS irritability, and sleeplessness; signs of toxicity include sinus tachycardia, failure to gain weight, vomiting, jitteriness, hyperreflexia, and seizures Caffeine citrate (Cafcit) Indications include AOP (eg, apnea after extubation from assisted ventilation, apnea after general anesthesia). Therapeutic index more favorable than that of aminophylline. Increases output of respiratory center, sensitivity of chemoreceptor to CO2, smooth muscle relaxation, and cardiac output. Serum half-life 40-230 h, which declines until 60-wk postmenstrual age. Dosing Adult Pediatric Loading dose: 20-40 mg/kg PO or IV over 30 min (equivalent to 10-20 mg/kg caffeine base) Maintenance dose: 5-8 mg/kg PO qd or slow IV bolus starting 24 h after loading dose (equivalent to 2.5-4 mg/kg caffeine base) Therapeutic trough serum concentrations 5-25 mcg/mL; measure trough levels 5 d after start of therapy; serum concentration >40-50 mcg/mL is toxic Interactions Antagonizes actions of adenosine; may reduce clearance of theophylline by 25% and cause additive pharmacologic effects (decrease dose); additive positive inotropic and chronotropic effects may occur with beta-adrenergic agonists; cimetidine and fluconazole decrease clearance, increasing serum levels; phenytoin induces hepatic metabolism, decreasing half-life and increasing clearance; increases metabolism of phenobarbital and increases own metabolism Incompatible with acyclovir, furosemide, lorazepam, oxacillin, and nitroglycerin Solution compatible with 5% or 10% dextrose in water and normal saline Terminal injection site compatible with dextrose and amino acid solutions, lipid emulsions, calcium gluconate, cefotaxime, cimetidine, clindamycin, dexamethasone, dobutamine, dopamine, epinephrine, fentanyl, gentamicin, heparin (<1 U/mL), isoproterenol, lidocaine, morphine, nitroprusside, pancuronium, penicillin G, phenobarbital, sodium bicarbonate, and vancomycin Contraindications Documented hypersensitivity; products containing sodium benzoate Precautions Pregnancy C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus Precautions May increase O2 consumption and decrease weight gain; do not administer dose if heart rate persistently >180 bpm; functional cardiac symptoms (eg, extrasystoles) possible; restlessness and vomiting can be signs of toxicity; cholestatic hepatitis may prolong serum half-life Follow-up Further Inpatient Care Apnea-free interval before discharge Most neonatologists agree that babies should be apnea-free for 2-10 days before discharge. However, the interval between the last apneic event and a safe time for discharge is not clearly established. The minimum apnea-free period is debated among clinicians. Darnall et al concluded that otherwise healthy preterm neonates continue to have periods of apnea separated by as many as 8 days before the last episode of apnea before discharge.123 Infants with long intervals between apneic event often have risk factors other than apnea of prematurity (AOP). Home monitoring Home monitoring after discharge is necessary for infants whose apneic episodes continue despite the administration of methylxanthine. Infants undergoing methylxanthine therapy rarely are sent home without a monitor because apnea may recur after they outgrow their therapeutic level. Without a monitor, caregivers may not know when apnea reappears. Some families cannot manage monitoring in the home. In these cases, the administration of caffeine may be the only possible therapy. Infants in this situation need frequent follow-up visits, and they should be readmitted for further evaluation when their blood levels approach the subtherapeutic range. Further Outpatient Care Home monitoring Various agencies and organizations have stated that home monitoring cannot prevent sudden infant death syndrome (SIDS), also called crib death or cot death, in preterm infants who have apnea of prematurity during their hospitalization.10,9 Indications for home monitoring Home monitoring may be indicated in the situations described below. Historical evidence suggests the occurrence of clinically significant apnea or an apparent life-threatening event (ALTE). Recording monitoring or multichannel evaluation documents apnea. The patient has gastroesophageal reflux (GER) with apnea. A sibling or twin of the patient died from SIDS or another postneonatal cause of death (see Special Concerns). The National Institutes of Health (NIH) consensus conference recommends monitoring for the siblings of infants with SIDS, but only after 2 SIDS-related deaths occur in a family. Physicians often begin monitoring after one sibling dies from SIDS; this practice may be related to a fear of litigation should another child in the family die from SIDS. Siblings of patients who died from SIDS are routinely monitored until one month past the patient's age at death. Monitoring is not indicated to prevent SIDS in infants older than one year, though proponents believe that such monitoring reduces anxiety in the parents of high-risk infants. Opponents of monitoring cite a lack of evidence to show that monitoring reduces the rate of SIDS. They argue that monitors intrude on the family's life and that they are poorly tolerated by the family.10 Types of monitors Several types of cardiorespiratory monitors are available for home use in the United States. The most common type combines impedance pneumography with an assessment of the patient's mean heart rate. The most notable drawback of impedance monitors is their inability to detect obstructive apnea. Newer monitors can minimize false alarms caused by motion artifact. Standard home monitors detect respiratory signals and heart rates. Electrodes are placed directly on the infant's chest or inside an adjustable belt secured around his or her chest. Monitoring units should be capable of recording cardiac and respiratory data because this information can help the physician in evaluating the need to stop medication or monitoring. These devices also record compliance with monitor use. The event recorder contains a computer chip that continuously records respiratory and cardiac signals. Normal signals are erased, but any event that deviates from preset parameters activates the monitor to save records of that event, as well as data 15-75 before and 15-75 seconds it. Additional channels are available to record pulse oximetry readings, nasal airflow, and body position (eg, prone vs supine). The records are downloaded within 24 hours after a parent reports an event or after excessive alarms occur. Many units now have computer modems that instantly transmit data to the physician's office for evaluation. These easily installed devices are especially useful for families who have had problems with events or alarms. Some devices, such as pulse oximeters, piezo belts, and pressure capsules, have been impractical to use or have had limited applications. Newer technologies and software programs may soon make such oximeters and similar devices more practical than they once were. All monitoring devices are associated with false alarms, which are alerts without in the absent of a true cardiorespiratory event. False alarms worry parents. If they happen often, they may discourage use of the monitor. Excessive false alarms can usually be minimized by adjusting the placement of the electrodes and by educating the parents. Details of monitoring depend on the frequency of events observed during neonatal hospitalization, the size and stability of the infant at the time of discharge, and the degree of parental anxiety. Follow-up of home monitoring and patient education Careful follow-up is needed with all cases of home monitoring in prematurely born neonates. Physicians who have limited experience with home monitoring or who cannot interpret the downloaded recordings should seek assistance from a center or program with expertise in these areas. The most important issue with monitoring is that Neonatal Resuscitation Program (NRP) instructors should educate parents, guardians, and other caregivers about neonatal resuscitation by using a mannequin before their child is discharged from the NICU. Parents should also be educated about prenatal and postnatal factors associated with an increased risk of SIDS, namely, the following:124,26 Prenatal and postnatal tobacco use Opiate abuse during pregnancy Baby's prone sleeping position Pacifier use Use of soft bedding Shared sleeping with children and adults Illnesses in infants with bronchopulmonary dysplasia Genetic factors Parents must also be aware that postural skull deformities have occurred after the AAP offered positioning recommendations in its Back to Sleep campaign.125 Prematurely born infants are probably at increased risk. Ways to avoid or minimize skull deformities should be discussed with parents. Parents of infants with home monitors must have a clearly designated person who they can contact on a regular basis and during emergencies. Many programs or centers provide 24-hour assistance for families of children with home monitors. The mean duration of home monitoring for prematurely born neonates is often more than 6 weeks. Extended monitoring is reserved for infants whose recordings show notable cardiorespiratory abnormalities. Monitoring beyond age 1 year is uncommon. Most often, children who require such monitoring have other conditions that require the use of additional technology. An example is an infant with bronchopulmonary dysplasia who requires mechanical ventilation at home. For infants who require therapy with a methylxanthine, drug therapy is typically stopped after 8 weeks without true events, but monitoring is continued for an additional 4 weeks.126,127 If no events are noted in this period, monitoring can be discontinued. These recommendations regarding discontinuing methylxanthines or home monitoring are not based on data from controlled studies; these investigations are badly needed. Complications Infants born prematurely are at increased risk for apnea and bradycardia after undergoing general anesthesia or sedation with ketamine, regardless of their history of apnea. Because of this increased risk, defer elective surgery, if possible, until approximately 52-60 weeks after conception to allow the infant's respiratory control mechanism to mature. Prognosis Regarding the natural history of apnea in infants born prematurely, the frequencies of all types of apnea gradually decreases during the first months of postnatal life. However, in some infants, apnea may persist until the age of 44 weeks after conception. Patient Education Family members and others involved in the care of an infant with apnea of prematurity should be well trained in cardiopulmonary resuscitation (CPR). Many of the pitfalls of home monitoring can be avoided by providing 24-hour telephone access (the ideal level of service) to a designated physician or nurse who is involved in the infant's care. In addition to this access, families should receive frequent, regularly scheduled telephone calls from healthcare providers, as well as home visits by a nurse or respiratory technician or follow-up appointments in a clinic familiar with this field of care. For excellent patient education resources, visit eMedicine's Children's Health Center. Also, see eMedicine's patient education article Sudden Infant Death Syndrome (SIDS). Miscellaneous Medicolegal Pitfalls An Internet search of the terms preterm infant, sudden infant death syndrome (SIDS), and malpractice yields results linked to several law practices. Some of these sites tell parents that they should sue over the SIDS-related death of their preterm infant. The medical literature is relatively silent about medical malpractice suits related to SIDS. The present authors know of malpractice cases involving infants who had apnea just days before discharge, who were discharged home without monitoring, and who then died at home or had an acute life-threatening event with brain injury. Even statements by national agencies that home monitoring cannot prevent SIDS have little impact when such malpractice cases go to a jury. When an unanticipated death does occur at home, it must be properly investigated. The investigation should address the possibility of death from child abuse, as well as late deaths from unrecognized malformations or inborn errors of metabolism (eg, fatty acid oxidation disorders).128 Special Concerns Controversies Related to Apnea of Prematurity Use of car seats or car beds The AAP has indicated that a car-seat challenge should be performed before preterm infants are discharged from the hospital.129 The importance of this testing is emphasized in an AAP pamphlet called Car Safety Seats: A Guide for Families 2007, which is given to parents. It addressed issues related to car-seat safety during infancy. Adverse events do happen when preterm infants are placed in car seats.130 However, authors of a Cochrane Review could not conclude whether car-seat testing with preterm infants was beneficial or detrimental. They did conclude that additional research was needed to evaluate its effectiveness in preventing the complications of apnea.131 If problems are found, treatment is another matter. Some have thought that if a preterm infant does not pass a car-seat challenge, they can be safely transported in a car bed. However, Salhab et al reported that apnea and other adverse events were as likely to occur in car beds as in car seats.132 A preterm infant riding in a car seat should be carefully observed by a caregiver. Retinal examinations In NICUs, preterm infants have had apneic events after retinal examinations. Although the drugs used to dilate the iris are implicated in these apneic events, the incidence and mechanisms associated with apnea have been poorly studied. Use of a pacifier Another belief is that a preterm infant is at increased risk for SIDS if they suckle a pacifier. Researchers have concluded that the opposite is true.133 Moreover, pacifiers do not affect breastfeeding in preterm infants.134 Pacifiers should obviously be removed from the mouth of a sleeping supine infant. Hypermagnesemia Studies reported decades ago demonstrated that hypermagnesemia secondary to maternal magnesium sulfate administration can cause apnea immediately after birth.72 Some neonatologists do not agree with this finding. Methylxanthine therapy Prophylactic versus intent-to-treat use of methylxanthines is another controversial subject. Some suggest prophylactic use of methylxanthines is indicated when very preterm infants are extubated to discontinue assisted ventilation. Older infants with a history of apnea of prematurity (AOP) may also benefit from prophylactic methylxanthines if they must undergo anesthesia for a surgical procedure. Likewise, prophylactic therapy with methylxanthines might seem reasonable in preterm infants with birth weights less than 1000 g. Nevertheless, use of methylxanthines in preterm infants are being viewed with caution because of their effects on brain development. Substantial disagreement exists among neonatologists regarding the criteria for stopping methylxanthine therapy, such as the numbers of days without apnea, bradycardia, or desaturation that are required. The discontinuation of methylxanthines may also depends on the patient's postconceptual age and other factors in an individual infant. Neonatologists are conflicted about what is considered safe in terms of the number of event-free days after a methylxanthine is stopped and the number of days without apnea before hospital discharge. Additional clinical research is urgently needed to resolve these issues. Use of caffeine versus aminophylline Despite the relatively broad therapeutic index, the use of caffeine versus aminophylline to treat AOP is still an unsettled issue with some neonatologists. Home monitoring To the authors' knowledge, no protocols to determine when a preterm infant with apnea of prematurity should or should not have home monitoring have been evaluated in clinical trials. Gastroesophageal reflux Despite the overwhelming body of evidence that gastroesophageal reflux (GER) is not associated with apnea, many neonatologists still use agents to inhibit gastric acidity and thereby prevent apnea. This controversial issue in preterm infants with apnea of prematurity has been discussed throughout this article. Sudden Infant Death SyndromeRelated Concerns Possible risk factors for SIDS or near-miss SIDS Infants born prematurely account for approximately 10% of the birth population, yet they experience slightly more than 20% of SIDS-related deaths. The immature respiratory control so commonly observed in premature neonates has led to suggestions of a relationship between apnea of prematurity and SIDS. Premature infants in NICUs often cease breathing unexpectedly. These events are frequently accompanied by bradycardia and O2 desaturation. In many instances, the infant might not have resumed breathing without direct intervention. The hypothesis that apnea is a cause of SIDS is attractive because the premature neonate does not struggle to resume breathing. This situation appears to be similar to that noted in many cases of SIDS. However, this theory of SIDS causation has not been proven. Furthermore, according to parental reports, most infants who died from SIDS were full-term neonates who had no apparent apneic events before death. However, visual detection of apnea and periodic breathing typically is difficult, even for medical personnel, and parents may miss such episodes. No evidence identifies apnea of prematurity as an independent risk factor for SIDS, despite the ongoing controversy surrounding the relationship between apnea and SIDS. Despite all of their common factors, large-scale trials conducted to verify the relationship between apnea of prematurity and SIDS have failed to delineate an abnormality of ventilatory control that underlies SIDS. Prolonged apnea has been reported in infants with near-miss SIDS (ie, infants who have had an apparent life-threatening event [ALTE]). Short episodes of apnea, periodic breathing, and mixed and obstructive apnea have been identified in infants with near-miss SIDS. These observations suggest that an abnormality in ventilatory control may contribute to SIDS. The risk of SIDS risk is highest among infants aged 2-4 months, similar to the risk for an ALTE. Positive family histories for these events are found for infants who die from SIDS and patients with apnea. Incidences of both conditions peak during cold weather months, and both typically occur while the infant is asleep. A reduction in postneonatal mortality and SIDS rates have been associated with sleeping in a supine position rather than a prone position. Several research groups have documented physiologic benefits with prone positioning versus supine positioning in preterm infants; advantages included a modest improvement in transcutaneously measured PO2, prolonged time in quiet sleep, decreased energy expenditure, and increased ventilatory responses to inspired CO2. However, recent studies indicated that prone sleeping may increase the risk of SIDS after hospital discharge.135,136 The increased risk of SIDS appears related to fewer arousals and more central apnea with prone versus supine sleeping. To decrease the incidence of SIDS, the AAP has recommended placing healthy neonates on their backs, instead of prone, for sleeping.124 The mechanism by which sleeping in the prone position can lead to SIDS is unclear. In the Nordic Epidemiological SIDS study, Oyen et al concluded that sleeping in both the prone and side positions increased the risk of SIDS. In addition, side-lying sleep could result in prone sleep.137 The risk is further increased among low-birth-weight infants, infants born before term, and infants aged 13-24 weeks. Soft bedding and shared sleeping are other factors related to SIDS. Posturing and cyanosis are often present, as is an increased incidence of prematurity, low birth weight, and evidence of poor prenatal care. Findings from epidemiologic studies suggest that as many as 18% of SIDS cases occur in infants who were born prematurely. Polygraphic monitoring for SIDS The aforementioned findings prompted the development of polygraphic monitoring to measure variables such as heart rate, nasal airflow, chest and abdominal movement, and transcutaneous O2 tension or O2 saturation to predict the risk for SIDS in vulnerable infants. A number of studies involving large cohorts of infants have not demonstrated that monitoring of cardiorespiratory variables can be used to prospectively identify infants at risk for SIDS. At present, no simple and accurate method is available to predict whether a premature infant is likely to die from SIDS. Home monitoring for SIDS At present, home monitoring is conducted in more infants born prematurely than in any other pediatric population. Each year, perhaps as many as 15-20% of the 400,000 premature babies are treated with home cardiorespiratory monitoring, primarily to manage apnea but also to prevent SIDS. Despite the number of premature infants receiving home monitoring, this therapy has not been embraced universally, and it remains controversial. Advocates believe that monitoring can alert caretakers to potentially serious episodes of apnea and/or bradycardia before they cause harm, helping parents to cope with the anxiety of caring for an infant born prematurely. Opponents cite the lack of evidence to indicate that monitoring alters the outcomes in any definable way. To the authors' knowledge, no prospective study has demonstrated that monitoring prevents SIDS. Furthermore, many physicians believe that the decision to use home monitoring places an emotional burden on parents. Many programs have been developed to enable home cardiorespiratory monitoring of prematurely born neonates to reduce the rate of SIDS. However, to the authors' knowledge, no prospective randomized control study has been conducted to show that home cardiorespiratory monitoring prevents SIDS. Anecdotal data from some programs suggest that the incidence of SIDS is lowered among premature neonates who are monitored extensively. However, the authors are aware of no data proving that home monitoring has caused this reduction in the incidence of SIDS. Also unclear is whether this approach is a cost-effective adjunct to neonatal care. Even programs that have reduced the incidence of SIDS have reported deaths among the babies who were monitored. Moreover, the cost of hospitalization has increased to such an extent that the expense of a single inpatient day may be as costly as several months of home cardiorespiratory monitoring. Ages of death In term neonates, the acknowledged peak age of death from SIDS is 2-4 months, with a mean age of 52 weeks after conception. The peak age of death for the premature infant is approximately 4-6 months, but the mean age of 52 weeks after conception is the same. Therefore, a premature neonate may be at risk for SIDS for a long period after hospital discharge. Little data are available regarding the comparative risks of SIDS among preterm neonates born at different postconceptional ages. The similarities in postconceptional ages of death for both term and preterm neonates suggests that a neurodevelopmental phenomenon may be among the etiologies of this as-yet unexplained problem. SIDS prevention Accumulating evidence from many countries indicates the importance of 2 factors for SIDS prevention in term infants: Placing infants supine for sleeping Preventing infants' exposure to cigarette smoke both during and after pregnancy Unless clear contraindications are present, treat premature neonates in a similar manner. These interventions appear to reduce the incidence of SIDS far more than home monitoring does. However, in some clinical situations, monitoring may be valuable to treat apnea of prematurity and to help families cope with the discharge of a low-birth-weight infant. NonSudden Infant Death Syndrome Monitoring Issues Since the introduction of NICUs, preterm neonates have received an extraordinarily high level of medical support to compensate for various degrees of organ immaturity at birth. Unfortunately, the effectiveness of current NICU technology cannot begin to approach the combined effectiveness of placental circulation and maternal metabolism. As a result, some premature babies survive, with different degrees of injury to certain organ systems. Bronchopulmonary dysplasia, cardiac disease, periventricular leukomalacia and other neurologic problems, and feeding difficulties are among the many problems that may require home monitoring for ongoing medical care. In these settings, monitoring appears valuable for alerting caretakers to any physiologic changes (eg, bradycardia, tachycardia, hypoxemia, seizures) that may require intervention. Without home monitoring, many infants might be hospitalized unnecessarily. The emotional and financial costs associated with such hospitalization may be far greater than those borne if they child and family were at home. In such instances, home monitoring may be an effective and safe approach to medical care. Home monitoring also may be an effective diagnostic tool for children whose events are so sporadic that they cannot be detected easily in the hospital. For example, newly developed monitoring devices can record abnormal events and can be used to detect and quantify infrequent episodes of apnea or ALTE, while helping to maintain a normal living situation for the child. If frequent events are detected, additional evaluation may be needed to identify a specific cause. Studies such as ECG, electroencephalography, cerebral imaging, and metabolic testing may be valuable in such instances. Whether the use of monitoring devices and/or pharmacologic agents (eg, methylxanthines) reduces apnea and improves neurodevelopmental outcomes in infants born prematurely is unknown. Because of the complex nature of the infant's medical problems, the contribution of apnea to any developmental disability is difficult to estimate but was suggested in recent publications.56 Frequent apnea may adversely affect neurodevelopmental outcomes, especially when it is accompanied by bradycardia and O2 desaturation, and it should be reduced or prevented if possible.138 Neonatologists are aware of the parents' anxiety when they take their low-birth-weight infant home. With recent changes in inpatient care, many premature babies now leave the hospital with discharge weights of 1800-2000 g. Home monitoring may help such infants make the transition to their home setting. Again, carefully train all caretakers who will care for the infant at home. Include instruction in the use of the monitor and in how to perform cardiopulmonary resuscitation (CPR). Of course, inform parents that monitoring might not prevent SIDS. 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Keywords apnea of prematurity, AOP, fetal breathing, pathologic apnea, central apnea, obstructive apnea, mixed apnea, apnea of infancy, AOI, neonatal apnea, sudden infant death syndrome, SIDS, crib death, cot death Contributor Information and Disclosures Author Dharmendra J Nimavat, MD, FAAP,Assistant Professor of Clinical Pediatrics, Department of Pediatrics, Division of Neonatology, Southern Illinois University School of Medicine Dharmendra J Nimavat, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics and American Association of Physicians of Indian Origin Disclosure: Nothing to disclose. Coauthor(s) Michael P Sherman, MD,Professor, Department of Child Health, University of Missouri-Columbia School of Medicine; Director, Fellowship Training Program in Neonatal-Perinatal Medicine, NICU, Columbia Regional Hospital; Professor Emeritus, Department of Pediatrics, University of California, Davis, School of Medicine Michael P Sherman, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, European Society for Paediatric Research, Perinatal Research Society, and Society for Pediatric Research Disclosure: Nothing to disclose. Rene L Santin, MD,Consulting Staff, Department of Pediatrics, Division of Neonatology, Primary Care Centers of Eastern Kentucky Disclosure: Nothing to disclose. Rachel Porat, MD,Director, Neonatal Apnea Monitoring Program, Assistant Director, Division of Neonatology, Albert Einstein Medical Center; Associate Professor, Department of Pediatrics, Thomas Jefferson University Rachel Porat, MD is a member of the following medical societies: American Academy of Pediatrics Disclosure: Nothing to disclose. Medical Editor Steven M Donn, MD,Professor of Pediatrics, University of Michigan Medical School; Director, Division of Neonatal-Perinatal Medicine, Department of Pediatrics, CS Mott Children's Hospital, University of Michigan Health System Steven M Donn, MD is a member of the following medical societies: American Pediatric Society Disclosure: Nothing to disclose. Pharmacy Editor Mary L Windle, PharmD,Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine Disclosure: Pfizer IncStockInvestment from financial planner;Avanir PharmaStockInvestment from financial planner ;WebMDSalary and stockEmployment and investment from financial planner Managing Editor Arun K Pramanik, MD, MBBS,Professor of Pediatrics, Director of Neonatal Fellowship, Louisiana State University Health Sciences Center Arun K Pramanik, MD, MBBS is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, National Perinatal Association, and Southern Society for Pediatric Research Disclosure: Nothing to disclose. CME Editor Carol L Wagner, MD,Professor of Pediatrics, Medical University of South Carolina Carol L Wagner, MD is a member of the following medical societies: American Academy of Pediatrics, American Chemical Society, American Medical Women's Association, American Public Health Association, American Society for Bone and Mineral Research, American Society for Clinical Nutrition, Massachusetts Medical Society, National Perinatal Association, and Society for Pediatric Research Disclosure: Nothing to disclose. Chief Editor Ted Rosenkrantz, MD,Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research Disclosure: Nothing to disclose. ./0ҽҟҽmU@U),h;!h;!0JCJOJQJ^JaJmH sH )h;!5B* CJ!KH$\aJ!mH ph3fsH /h;!h;!5B* CJ!KH$\aJ!mH ph3fsH 1h;!h;!B*CJOJQJ^JaJmH phsH 1h;!h;!B* CJOJQJ^JaJmH phfsH :jh;!h;!B* CJOJQJU^JaJmH phfsH (h;!h;!CJOJQJ^JaJmH sH 1jh;!h;!CJOJQJU^JaJmH sH (h;!h;!CJOJQJ^JaJmH sH    * 5 ` }}iidx-D@&M gd;!d&d -D@&M P3fgd;!KKx-DM [$\$]K^Kgd;!KKK-DM [$\$]K^Kgd;!-D@&M gd;!&d -D@&M P3fgd;!dgd;! p / @   * ` -/$0L뿧zdzdzdzdzdzLz.h;!h;!5CJOJQJ\^JaJmH sH +h;!h;!CJH*OJQJ^JaJmH sH (h;!h;!CJOJQJ^JaJmH sH .h;!h;!5CJOJQJ\^JaJmH sH /h;!h;!5B* OJQJ\^JmH ph3fsH )h;!5B* OJQJ\^JmH ph3fsH ,h;!h;!0JCJOJQJ^JaJmH sH (h;!h;!CJOJQJ^JaJmH sH ` 0$h;js$0Mdx-D@&M gd;! 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