Characterization of the response to primary blast injury

Abstract

Lung injuries, predominantly arising from blast exposure, are a clinical problem in a significant minority of current military casualties. This special feature consists of a series of articles on lung injury. This first article examines the mechanism of the response to blast lung (primary blast injury to the lung). Subsequent articles examine the incidence of blast lung, clinical consequences and current concepts of treatment, computer (in silico) modelling of lung injury and finally chemical injuries to the lungs. Blast lung is caused by a shock wave generated by an explosion causing widespread damage in the lungs, leading to intrapulmonary haemorrhage. This, and the ensuing inflammatory response in the lung, leads to a compromise in pulmonary gas exchange and hypoxia that can worsen over several hours. There is also a characteristic cardio-respiratory effect mediated via an autonomic reflex causing apnoea (or rapid shallow breathing), bradycardia and hypotension (the latter possibly also due to the release of nitric oxide). An understanding of this response, and the way it modifies other reflexes, can help the development of new treatment strategies for this condition and for the way it influences the patient's response to concomitant injuries.

Blast Injuries

“…The pathophysiology includes capillary rupture within the alveoli, which leads to hemorrhage and pulmonary edema. This ultimately reduces gas exchange, causing both hypoxia and hypercarbia (1,11,27,28).…”

Blast injury: A case study

“…The process is known as spalling and when it affects the lungs it can result in a condition known as Blast Lung, and is the most common cause of PBI death. Blast Lung is characterised by the rupture of alveoli capillaries and the subsequent influx of blood and development of pulmonary oedema, which leads to a reduction in pulmonary gas exchange with subsequent hypoxia and hypercarbia (Kirkman and Watts, 2011;Bridges, 2006;Rosenfeld and Ford, 2010). Blast Lung leads to the development of acute respiratory failure and can occur within minutes (Bridges, 2006), but a late presentation can also occur 24-48 h later (Chaloner, 2005).…”

“…Indeed it is possible that a casualty can have little or no obvious external injuries, as supported by Kluger (2003) where clear data has been generated from the Israeli-Palestinian conflict. Kirkman and Watts (2011) states observations from the First World War pertaining to casualties who developed shock despite no obvious external injuries. Therefore the rationale for including this particular casualty as a case study is despite a left sided tension pneumothorax, he had not sustained any external injury.…”

Development of an Animal Model for Burn-Blast Combined Injury and Cardiopulmonary System Changes in the Early Shock Stage

“…The effects were also reflected in important pathophysiological processes. In many cases, the compounded effect of the combined injury was "mutually aggravating," which can contribute to the difficulty of curing the wound [16]. Burn-blast combined injury is one of the common injuries both during war and peacetime.…”