PEDIATRICS Vol. 106 No. 5 November 2000, pp. 1135

COMMENTARY:
Commentary on Surfactant Treatment of Neonates With Respiratory Failure and Group B Streptococcal Infection

There were concerns about adverse effects of treating infants with sepsis/pneumonia during the initial trials of surfactant for infants with respiratory distress syndrome (RDS). It is not possible to reliably distinguish preterm infants with group B streptococcal sepsis/pneumonia (who also may be surfactant-deficient) from infants with RDS within minutes to hours of birththe time frame that is optimal for surfactant treatments. Anecdotal reports suggested no harm from treating infected preterm infants with surfactant. Subsequent trials of surfactant treatment of term infants with severe respiratory failure (many of whom were infected) demonstrated benefit.^1,2 Therefore, clinical practice is to treat preterm infants who appear to have RDS with surfactant and antibiotics and to sort out subsequently and imperfectly RDS from infection. The treatment of severe respiratory failure in term infants with surfactant also is common. In this month's issue of Pediatrics, Herting et al³ provide valuable information about the surfactant responses of 118 infants infected with group B streptococcus in comparison to the surfactant responses of infants with RDS. The authors emphasize the less striking and somewhat delayed oxygenation response as compared with the surfactant treatment response of infants with RDS. About 25% of the infected infants did not have an acute improvement in oxygenation. In contrast, I am impressed that many of the infected infants responded to surfactant treatment as well as they did. As with the clinical response to surfactant of infants with meconium aspiration, a more gradual improvement was apparent.

The authors do not tell us if the improvement in oxygenation with surfactant treatment predicted outcomes. Group B streptococcal infection is a serious disease, and as anticipated, there were more deaths and adverse outcomes for the infected infants than for the infants with RDS. I would like to know how many of the 30% of the infected infants who died were included in the 25% who did not respond to surfactant. Oxygenation problems in infants with group B sepsis/pneumonia can result from a relative surfactant deficiency, presumably from surfactant inactivation from proteinaceous pulmonary edema.⁴ However, myocardial dysfunction and pulmonary hypertension also cause hypoxia. It would be helpful to know if the absence of an oxygenation response to surfactant identifies the infants with cardiovascular causes for the high oxygen needs.

The concerns that surfactant can promote infection fortunately have not occurred clinically. Natural surfactant contains innate host defense factors such as defensins and lysozyme as well as the surfactant proteins.^5,6 SP-A and SP-D are collectins that bind endotoxin, bacteria, yeast, and viruses and promote phagocytosis and killing. These proteins also can modulate the inflammatory response to an infectious stimulus and decrease granulocyte recruitment to and proinflammatory cytokine expression in the lungs.⁷ Most of the infants reported by Herting et al were treated with surfactant isolated from animal lungs, and the processing required for clinical use removes the host defense factors. The hydrophobic surfactant proteins SP-B and SP-C may have some host defense functions. An attractive research goal is to develop surfactants with host defense functions that should be helpful for the treatment of infected lungs and might mitigate the severe proinflammatory responses that no doubt contribute to bronchopulmonary dysplasia. Twenty percent of the group B streptococcal-infected infants ended up with bronchopulmonary dysplasia. The value of the Herting article is to demonstrate clearly that there should be no concerns about treating preterm or term infants with sepsis/pneumonia syndromes and respiratory failure with surfactantthe treatment will not hurt and it will help about 70% of the time.

Alan H. Jobe, MD, PhD
Neonatal/Pulmonary Biology
Children's Hospital Medical Center
Cincinnati, OH 45229-3039

FOOTNOTES

Received for publication May 8, 2000; accepted May 8, 2000.

Address correspondence to Alan H. Jobe, MD, PhD, Children's Hospital Medical Center, Division of Pulmonary Biology, 3333 Burnet Ave, Cincinnati, OH 45229-3039. E-mail: jobea0{at}chmcc.org

ABBREVIATIONS

RDS, respiratory distress syndrome.

REFERENCES

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