Is it rational to treat pneumonia with exogenous surfactant?

Pneumonia is an important cause of respiratory failure, and is associated with increased alveolar permeability leading to pulmonary oedema, haemorrhage and atelectasis [1, 2]. The pathophysiological changes in pneumonia include hypoxaemia, decreased functional residual capacity (fRC), decreased total lung capacity (TLC), decreased lung compliance, and a diminished surfactant system [3-5]. As early as 1964, SlJINICK and SoLOFF [1] demonstrated that the surface tension of bronchoalveolar lavage (BAL) fluid from lung tissue with pneumonia was increased. They suggested that the pulmonary surfactant became inactivated and was responsible for atelectasis. Since then, it has been demonstrated that the surfactant system is impaired in bacterial [5], and viral pneumonia [6], as well as in Pneumocystis carinii pneumonia [7, 8]. These observations are based on the following findings. In bacterial pneumonia, surface tension of BAL fluid is increased. whereas surfactant protein A (SPA) content, total surfactant-lipids, the lecithin/sphingomyelin ratio, phosphatidylglycerol (PG), phosphatidylcholine (PC), and the amount of palmitic acid in PC, are all signilicantly decreased [5, 9]. Morphological changes in type ll pneumocytes, which produce surfactant have been observed [2], and one could expect that surfactant of normal composition is no longer synthesized. In viral pneumonia, STINSON et al. [6] demonstrated that pulmonary surfactant activity is decreased. These workers suggested that injury and destruction of type II pneumocyteS by the virus were the cause of reduced surfactant activity, and may contribute to pulmonary collapse. Recently, surfactant abnormalities have been demonstrated in human immunodeficiency virus (HIV) positive patients with Pneumocystis carinii pneumonia [7, 8]. In these patients qualitative and quantitative changes were seen in the surfactant composition, as well as increased phospholipase ~ activity [8]. It is known that pulmonary surfactant is a carpet of lipids and specific proteins coating the interior of the lung, thus preventing end-expiratory collapse of the alveoli and small airways [10]. An intact surfactant system is also essential to maintain the fluid balance in the lung [11]. Destruction or inactivation of the surfactant results in alveolar collapse and pulmonary oedema [ 12]. It has also been demonstrated that surfactant plays a role in the lung's defence against infection (13]. In addition, surfactant, and in particular SPA , enhance the antibacterial and antiviral defence of alveolar macrophages [13]. Bacteria, bacterial toxins, viruses, phospholipases and proteinases released from inflammatory cells interact either directly with the surfactant film, or damage the endothelial and epithelial cells, leading to high permeability oedema [5, 14]. It …