In 1959, not long after surfactant had been identified as critical to maintaining lung inflation at low transpulmonary pressures,1,2 Avery and Mead3 reported that saline extracts from the lungs of preterm infants with respiratory distress syndrome lacked the low surface tension characteristic of pulmonary surfactant. After several unsuccessful attempts to treat infants with respiratory distress syndrome with aerosolized surfactant,4,5 intratracheal administration of surfactant recovered from the air spaces of mature animal lungs was found to improve lung expansion and ventilation in preterm animals6–8. The clinical potential of surfactant treatment for respiratory distress syndrome was demonstrated by . . .

Pulmonary surfactant therapy.

Pulmonary surfactant is a complex and highly surface active material composed of lipids and proteins which is found in the fluid lining the alveolar surface of the lungs. Surfactant prevents alveolar collapse at low lung volume, and preserves bronchiolar patency during normal and forced respiration (biophysical functions). In addition, it is involved in the protection of the lungs from injuries and infections caused by inhaled particles and micro-organisms (immunological, non-biophysical functions). Pulmonary surfactant can only be harvested by lavage procedures, which may disrupt its pre-existing biophysical and biochemical micro-organization. These limitations must always be considered when interpreting ex vivo studies of pulmonary surfactant. A pathophysiological role for surfactant was first appreciated in premature infants with respiratory distress syndrome and hyaline membrane disease, a condition which is nowadays routinely treated with exogenous surfactant replacement. Biochemical surfactant abnormalities of varying degrees have been described in obstructive lung diseases (asthma, bronchiolitis, chronic obstructive pulmonary disease, and following lung transplantation), infectious and suppurative lung diseases (cystic fibrosis, pneumonia, and human immunodeficiency virus), adult respiratory distress syndrome, pulmonary oedema, other diseases specific to infants (chronic lung disease of prematurity, and surfactant protein-B deficiency), interstitial lung diseases (sarcoidosis, idiopathic pulmonary fibrosis, and hypersensitivity pneumonitis), pulmonary alveolar proteinosis, following cardiopulmonary bypass, and in smokers. For some pulmonary conditions surfactant replacement therapy is on the horizon, but for the majority much more needs to be learnt about the pathophysiological role the observed surfactant abnormalities may have.

https://erj.ersjournals.com/content/erj/13/6/1455.full.pdf

Pulmonary surfactant in health and human lung diseases: state of the art.

Pulmonary surfactant in health and human lung diseases: state of the art

Respiratory failure secondary to surfactant deficiency is a major cause of morbidity and mortality in preterm infants. Surfactant therapy substantially reduces mortality and respiratory morbidity for this population. Secondary surfactant deficiency also contributes to acute respiratory morbidity in late-preterm and term neonates with meconium aspiration syndrome, pneumonia/sepsis, and perhaps pulmonary hemorrhage; surfactant replacement may be beneficial for these infants. This statement summarizes indications, administration, formulations, and outcomes for surfactant-replacement therapy. The impact of antenatal steroids and continuous positive airway pressure on outcomes and surfactant use in preterm infants is reviewed. Because respiratory insufficiency may be a component of multiorgan dysfunction, preterm and term infants receiving surfactant-replacement therapy should be managed in facilities with technical and clinical expertise to administer surfactant and provide multisystem support.

https://pediatrics.aappublications.org/content/pediatrics/121/2/419.full.pdf

Surfactant-Replacement Therapy for Respiratory Distress in the Preterm and Term Neonate

Surfactant for the treatment of respiratory distress syndrome

To the Editor.— Sinkin and co-workers1 undertook the laudable goal of attempting to predict the risk of "bronchopulmonary dysplasia" (defined solely as a requirement for supplemental oxygen at 28 days) to select better infants who might benefit from interventions to reduce the frequency of this chronic lung disease. Other investigators have defined risk of bronchopulmonary dysplasia (BPD) in the first days to weeks of life using similar statistical analyses,2,3 cytopathology,4 detection of elevated proteases in airway secretions,5-7 measurement of airways mechanics,8,9 and clinical and radiographic scores.10,11

The BPD Problem

The present study was undertaken to determine if a synthetic peptide, KLLLLKLLLLKLLLLKLLLLK (KL4), in which K = lysine and L = leucine, in an aqueous dispersion of phospholipids (DPPC and POPG), would expand pulmonary alveoli and improve gas exchange in premature human infants with respiratory distress syndrome (RDS). The KL4 peptide was synthesized to resemble the amino acid pattern of surfactant protein B (SP-B). Forty-seven infants with RDS were treated within 4 h of birth with the KL4-peptide/phospholipid mixture, called KL4-Surfactant. The average arterial-to-alveolar oxygen tension ratios (a/A O2) of 39 patients included in efficacy analyses rose from pretreatment values of 0.14 +/- 0.02 (mean +/- SEM) to 0.40 +/- 0.04 (normal value > or = 0.40) by 12 h of age. Mean airway pressures and oxygenation index values fell concomitantly, and expansion of the lungs was observed on radiographs. The median duration of mechanical ventilation was 5.0 d. Of the 39 included infants, 29 required only a single dose. Radiographic data indicate that those patients requiring a second instillation of KL4-Surfactant but not showing a sustained rise in a/A O2 ratios did, in fact, exhibit expansion of alveoli in the lung. There were no RDS-related deaths; the incidence of complications was no higher than found in other comparable published studies. The data demonstrate that the synthetic peptide, KL4, which mimics the hydrophobic and hydrophilic pattern of SP-B, when formulated in an aqueous dispersion with the phospholipids DPPC and POPG, creates a strong and durable surfactant activity as judged by expansion of pulmonary alveoli and improvement of gas exchange in infants with RDS.

The efficacy and safety of KL4-surfactant in preterm infants with respiratory distress syndrome.

Chest radiographs of 18 newborns treated with endotracheal instillation of human surfactant for respiratory distress syndrome (RDS) were compared with those of 18 similar but untreated infants. In the treated infants, severity of RDS significantly improved after surfactant administration. Most treated infants (16/18) exhibited a left-to-right shunt, presumably through a patent ductus arteriosus; similar findings were noted in untreated infants (17/18). Complications of respiratory assistance in the treated infants included transient pulmonary interstitial emphysema (n = 1), pneumothorax (n = 1), and mild (n = 4) to moderate (n = 2) bronchopulmonary dysplasia; the incidences of these complications did not exceed those in untreated infants. In three treated infants, a transient interstitial lung disease developed 3-4 days after surfactant administration.

Respiratory distress syndrome treated with human surfactant: radiographic findings.

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The BPD Problem

The efficacy and safety of KL4-surfactant in preterm infants with respiratory distress syndrome.

Respiratory distress syndrome treated with human surfactant: radiographic findings.