For Healthcare Providers

Candidates for RSV Prophylaxis

Premature Infants

  • Infants born prematurely represent a large group at high risk for complications due to a severe respiratory syncytial virus (RSV) disease.1
  • Although many premature infants appear healthy, studies show that they may suffer from interrupted lung development, and immature immune systems.2-3
  • All infants born at 35 weeks or less gestation are at a significantly elevated risk for severe RSV disease.4

Premature Infants: Immature Immune System

  • As a result of being born prematurely, infants born before 36 weeks' gestation possess significantly less maternally-transmitted antibody (IgG).5
  • Additionally, premature infants are further compromised by deficient cellular immunity.6
  • As a result, premature infants have less protection against pathogens like RSV.

Premature Infants Have Lower Immunoglobulin (IgG) Levels at Birth Compared with Term Infants5

Lower serum antibody levels increase the risk for severe RSV disease.
  • The transfer of maternal antibodies to the fetus predominantly occurs after the 28th week of pregnancy. Premature birth interrupts this transfer, leading to lower levels of maternally-transmitted antibody at birth. As a result, infants born prematurely have significantly less protection from RSV infections compared to full-term infants at birth, even 32-35 week GA infants.3
  • The immune systems of premature infants are further compromised by deficient cellular immunity.4 Cellular immunity in young infants can permit more pronounced viral replication and altered immune response, resulting in more extensive disease and damage to the already-compromised and altered airways.

Premature Infants: Interrupted Lung Development

  • A premature infant is at high risk for severe RSV disease due, in part, to an underdeveloped pulmonary system.

32-35 week GA infants are within the same stage of lung development as 28-32 week GA infants6

Stages of lung development

Premature Infants: Underdeveloped Lungs at Birth

Why are 32-35 week GA infants so vulnerable?

Estimates of lung capacity and structure at birth

Reduced airway function is seen in 32-35 week GA infants at 1 year8-10

Graph of premature infants: Lung function at 1 year

Premature Infants: Altered Lung Development

  • A premature infant is at high risk for severe RSV disease due, in part, to an underdeveloped pulmonary system
  • At birth, the lungs of a premature infant have significantly decreased volume and surface area, and increased airspace wall thickness, further inhibiting gas exchange.
  • When this immature lung is exposed to the requirements of breathing with higher oxygen levels and mechanical stress, subsequent airway and alveolar development is significantly altered.9,11
Bronchiole of premature infant with RSV
  • The premature lung has decreased airway diameters7 (contributing to increased airway resistance).
  • Despite the fact that many premature infants appear healthy, it has been observed that abnormal airway development in premature infants leads to a significant reduction in lung function at 1 year of age.9
  • As a result of altered airway development and the resulting decrease in lung function, RSV lower respiratory tract infections are likely to cause more severe disease.
Still image from immature immune system video in premature infants.
  • View an educational video clip about the immature immune system in premature infants.
  • Click here for a high-resolution version.
  • To download the files to your computer, right click on the "View" link, and then select the "Save Target As..." option.

Important Safety Information

Synagis® (palivizumab) is indicated for the prevention of serious lower respiratory tract disease caused by respiratory syncytial virus (RSV) in pediatric patients at high risk of RSV disease and is administered by intramuscular injection. Safety and efficacy were established in infants with bronchopulmonary dysplasia (BPD), infants with a history of premature birth (≤35 weeks gestational age), and children with hemodynamically significant congenital heart disease (CHD). Synagis has been used in more than one million children in the U.S. since its introduction in 1998. The first dose of Synagis should be administered prior to commencement of the RSV season. Patients, including those who develop an RSV infection, should continue to receive monthly doses throughout the season.

Synagis should not be used in pediatric patients with a history of severe prior reaction to Synagis or its components. Cases of anaphylaxis were reported following re-exposure to Synagis and severe acute hypersensitivity reactions have also been reported on initial exposure or re-exposure. If a severe hypersensitivity reaction occurs, therapy with Synagis should be permanently discontinued. If milder hypersensitivity reactions occur, caution should be used on re-administration of Synagis. In post-marketing reports, cases of severe thrombocytopenia (platelet count <50,000/microliter) have been reported.

In clinical trials, the most common adverse events occurring at least 1% more frequently in Synagis-treated patients than controls were upper respiratory infection, otitis media, fever, and rhinitis. Cyanosis and arrhythmia were seen in children with CHD. There have also been post-marketing reports of injection site reactions.

Click here for full Prescribing Information.

References

  1. Meissner HC. Pediatr Clin N Am. 2005;52:695-710.
  2. Moore KL, Persaud TVN. The Developing Human: Clinically Oriented Embryology. 7th ed. Philadelphia, Pa: Saunders; 2003:245-251.
  3. Langston C, Kida K, Reed M, et al. Am Rev Respir Dis. 1984;129:607-613.
  4. Boyce TG, et al. Rates of hospitalization for respiratory syncytial virus infection among children in Medicaid. J Pediatr: 2000; 137:865-870.
  5. Yeung CY, Hobbs JR. Lancet. 1968;1:1167-1170.
  6. Bont L, Kimpen JL. Intensive Care Med. 2002;28:616-621.
  7. Hacimustafaoglu M, Celebi S, Aynaci E, et al. Arch Dis Child. 2004;89:52-53.
  8. Hoo A-F, Dezateux C, Hanrahan JP, Cole TJ, Tepper RS, Stocks J. Am J Respir Crit Care Med. 2002;165:1084-1092.
  9. Hoo A-F, Dezateux C, Henschen M, J Pediatr. 2002;141:652-658.
  10. Data on file at MedImmune, LLC.
  11. Hjalmarson O, Sandberg K. Am J Respir Crit Care Med. 2002;165:83-87.
  12. Hall CB, N Engl J. Med. 2001;344;1917-1928
View Important Safety Information