The concept of activated leukocytes adhering to endothelium and then migrating to release their contents in the tissues is evidently a useful model, but it is not the sole explanation of multiple organ failure. Platelets can contribute to cellular or organ injury by the formation of platelet plugs and distal ischemia, and also by promoting neutrophil activation and adhesion. Activated neutrophils become more rigid, and may also cause microvascular occlusion, shunting, and tissue ischemia independent of direct chemical injury. Activated neutrophils will adhere to endothelium, but may not migrate into the tissues unless the endothelium has been stimulated by the additional presence of cytokines such as interleukin 8 (IL-8). Many cytokines promote leukocyte adhesion, and the variability of clinical presentation of multiple organ failure may be a consequence of variable expression by different organs of these chemotactic cytokines, some of which may be produced by injured tissue which then becomes the target of secondary attack. For example, a patient with a prior respiratory infection may be more likely to develop acute respiratory failure following an emergency surgical procedure simply because of pulmonary cytokine signaling.
The flow characteristics in certain organs will also influence the presentation of multiple organ failure, with renovascular disease being an obvious example. Accumulation of toxins, drugs, or active drug metabolites may explain the predominance of certain organ failures such as encephalopathies or renal dysfunction.
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