Commercial Air Travel by Prematurely Born Infants
Commercial Air Travel by Prematurely Born Infants
Abstract and Commentary
By Tyler Hartman, MD, Jonathan Johnson, MD, & Philip R. Fischer MD, DTM&H
Drs. Hartman and Johnson are Residents, Department of Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, MN, and Dr. Fischer is Professor of Pediatrics, Division of Pediatric and Adolescent Medicine, Mayo Clinic
Drs. Hartman, Johnson, and Fischer report no financial relationships relevant to this field of study.
Synopsis: Young, prematurely-born infants with neonatal lung disease are at high risk of oxygen desaturation during commercial air travel. Hypoxia testing, if possible prior to air travel, or deferral of long air trips, should be considered for young infants with neonatal lung disease, even if they are not requiring oxygen.
Source: Udomittipong K, et al. Pre-flight testing of preterm infants with neonatal lung disease: A retrospective review. Thorax. 2006; 61:343-347.
Increasingly, infants with a history of neonatal lung disease are traveling by air. With advancing technology, aircraft are able to fly longer distances at higher altitudes. Due to limitations in aircraft structure, planes at cruising altitude can only be pressurized to the equivalent of 6,500 ft above sea level, resulting in a lower partial pressure of cabin oxygen. In 2004 the British Thoracic Society (BTS) updated their air travel guidelines for infants and young children with a history of respiratory disease, stating that an in-flight blood oxygen saturation of < 90% was an indication for supplemental oxygen. Studies have shown that healthy, term infants drop their oxygen saturation by 4-5% during hypoxia tests with 15-16% oxygen, and more than 10% of these healthy infants have significant blood oxygen desaturations to below 80%.1
Udomittipong and colleagues recently conducted a retrospective chart review of 47 infants with a history of neonatal chronic lung disease (nCLD). These infants were no longer requiring supplemental oxygen, had baseline oxygen saturations > 95%, and were referred for a hypoxia test to determine fitness to fly. The hypoxia test consisted of exposure to 14-15% oxygen for approximately 20 minutes with concurrent saturation monitoring. Of the infants tested, 81%, predominantly younger than 1 year of age, desaturated to below 85%, indicating the need for in-flight supplemental oxygen. Infants that passed the hypoxia test were significantly older than those who did not, averaging a corrected (post-due date) age of 12.7 months. The authors' conclusion was that infants younger than 12 months (corrected age) with a history of nCLD are at high risk for desaturation during commercial flights. They recommended that these infants be screened with hypoxia testing prior to traveling to determine need for supplemental oxygen.
Commentary
The study by Udomittipong et al considered a blood oxygen desaturation during the hypoxia test to < 85% as indicative of need for oxygen supplementation during air travel. The BTS recommends supplementation if there is a desaturation to below 90%, which is significantly more conservative. Therefore, the 81% of the infants in this study that would require in-flight supplemental oxygen is possibly an underestimation. The hypoxia test done in this study was approximately 20 minutes in length, which is considerably shorter than most commercial airline flights. Lee et al have shown a continued decrease in blood oxygen saturations occurring from 3 hours to 7 hours into air travel in population of healthy 6-month to 14-year-old children who are much less susceptible to desaturation.2 The data suggest that Udomittipong's study may underestimate the necessity for supplemental oxygen in infants with a history of nCLD.
Several studies have shown that most people average a 4% decrease in their blood oxygen saturation during commercial airline flights. This is usually clinically insignificant for healthy children and adults. There are many reasons why former premature infants are likely to be more susceptible to in-flight desaturation, even with mild lung disease and when clinically stable on room air. High altitude pulmonary edema has been linked to an individual's tendency to respond to hypoxia with an abnormal increase in pulmonary artery pressure. Infants with a history of chronic lung disease are at risk of elevated pulmonary artery pressures with normal oxygen levels. Theoretically, these infants have a higher risk of pulmonary edema and respiratory compromise with hypoxia than infants with normal pulmonary artery pressures.3 Premature infants have been shown to have a persistence of biphasic ventilatory response to hypoxia, resulting in a sustained decrease in respiratory frequency.4 Unlike term infants who have been shown to have a decrease in apnea when hypoxic, infants with a history of prematurity show an increase in both the frequency and duration of apneas,5 even after discharge from the hospital.4 Although it seems logical that premature infants should be at a greater risk for significant desaturations when exposed to hypoxic conditions, there has been little direct evidence to support this claim.
The clinical consequences of transient drops in an infant's oxygen saturation remain uncertain. In 1998 British investigators examined the administration of 15% oxygen to healthy term infants and reported an increase in irregular breathing and desaturations.1 The authors suggested that airway hypoxia may be responsible for the anecdotal connection between commercial airline travel and Sudden Infant Death Syndrome (SIDS). The media inflated the very weak evidence supporting this claim, which resulted in public overreaction. The plausible physiologic bases for this claim have not been supported by the epidemiologic evidence. There have been no studies, prospective or retrospective, that have supported this claim. There have, however, been conflicting studies that have examined the relationship between high altitude and SIDS. Two studies in the United States6,7 and one study in Austria8 have indicated a significant increase in the incidence of SIDS at high altitudes; however, a study in Colorado showed high altitude is not an independent risk factor for SIDS.9 Even though cabin oxygen content during a commercial airline flight is the equivalent being at 6,500 feet of altitude, these studies cannot be generalized to this population due to the transient nature of air travel. The UK's Confidential Inquiry into Stillbirths and Deaths in Infants (CESDI 1995–1996) found none of the 130 case of SIDS had recently flown.10 None of these studies examined the incidence of SIDS in infants with a history of prematurity and nCLD, as these patients are at higher risk of SIDS already.
The evidence that commercial air travel is a significant risk factor for SIDS in healthy term neonates is not strong enough to recommend that this population should not fly. The present study, however, indicates that infants with a history of nCLD are more likely to have significant oxygen desaturation and require oxygen during air travel. This study likely underestimates the need for oxygen supplementation suggested by the BTS 2004 guidelines in order to maintain "adequate" oxygen saturation. The clinical significance of desaturation below 85% in this population has yet to be determined and, until further information is available, it is safer to err on the side of caution. We suggest that any infant younger than 12 months of age with a history of nCLD, regardless of current oxygen saturation, should undergo a hypoxia test equal to the duration of the upcoming flight. When this is not possible, it may be prudent to delay air travel until after 12 months of age or simply have supplemental oxygen prescribed prior to departure.
References:
- Parkins KJ, et al. Effect of exposure to 15% oxygen on breathing patterns and oxygen saturation in infants: Interventional study. BMJ. 1998;316:887-891.
- Lee AP, et al. Commercial airline travel decreases oxygen saturation in children. Pediatr Emerg Care. 2002;18:78-80.
- McCurnin DC, et al. Inhaled NO improves early pulmonary function and modifies lung growth and elastin deposition in a baboon model of neonatal chronic lung disease. Am J Physiol Lung Cell Mol Physiol. 2005;288:L450-L459.
- Martin RJ, et al. Persistence of the biphasic ventilatory response to hypoxia in preterm infants. J Pediatr. 1998;132:960-964.
- Rigatto H, Brady JP. Periodic breathing and apnea in preterm infants. II. Hypoxia as a primary event Pediatrics. 1972;50:219-228.
- Getts AG, Hill HF. Sudden infant death syndrome: Incidence at various altitudes. Dev Med Child Neurol. 1982;24:61-68.
- McCullough RE, et al. Fetal growth retardation and increased infant mortality at high altitude. Obstet Gynecol Surv. 1977;32:596-598.
- Kohlendorfer U, et al. Living at high altitude and risk of sudden infant death syndrome. Arch Dis Child. 1998;79:506-509.
- Barkin RM, et al. Influence of high altitude on sudden infant death syndrome. Pediatrics. 1981;68:891-892.
- Platt MP, et al. Hypoxic responses in infants. Danger to babies from air travel must be small. BMJ. 1998;317:676. Author reply: 677-678.
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