ABSTRACT
ARDS can be considered to be the respiratory component to the multiorgan effects of the systemic inflammatory response syndrome or SIRS (see ‘Sepsis and SIRS’, Chapter 121, page 505). An acute inflammatory response is seen with an immediate exudative phase, involving activated neutrophils and activated macrophages secreting a number of cytokine mediators of acute inflammation, including interleukin 6 (Il-6), tumour necrosis factor (TNF), proteases, prostaglandins and oxygen radicals. In turn, the complement system is activated along with local activation of the clotting cascades. This increases capillary permeability by local endothelial injury, manifesting as a decrease of type II pneumocytes and reduced pulmonary surfactant production.This reduces lung compliance further by increasing the force required to open the alveoli.
