Abstract

To facilitate effective gas exchange and act as a blood-gas interface the adult human lung consists of some 500 million air sacs (alveoli), each only 1/3 mm in diameter but generating a combined surface area of approximately 100 m2. The alveolar wall measures 0.2–0.3 μm across and is encased in a mesh of very fine and fragile blood vessels the diameter of which is just sufficient to allow the passage of red blood cells [1]. Whilst elegantly adapted to facilitate rapid diffusion of gas across tissue, the very nature of the lungs’ role in gas exchange renders them particularly susceptible to injury following blast exposure. Such injury, due only to exposure to blast wave (primary blast) and not to other consequences of proximity to an explosion (for example penetrating – secondary blast – or burn injuries – quaternary blast) is known as primary blast lung injury (PBLI). As a diagnosis of exclusion, it occurs within 12 h of blast exposure in the absence of secondary or tertiary lung injury and in the presence of radiological or arterial blood gas evidence of acute lung injury [2].

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