Timothy W. Evans – författare

A huge amount of research has focused on the mechanisms of acute lung injury and yet the exact sequence of events and media tors in inflammatory cascade, which result in acute respiratory failure from ARDS, is not known but many possibilities exist.

Great progress has been made since the first description of the acute respiratory distress syndrome by the Denver group in 1967 (Lancet). Although we introduced the term ''adult respiratory distress syndrome'' in our second and more detailed description of the syndrome (ehest, 1971), this was probably amistake for the simple reason that children also suffer the same syndrome fo11owing acute lung insults. Today, the syndrome of acute respiratory distress in adults (ARDS) is recognized as a worldwide problem, but the prevalence of disease varies in different parts of the world. A huge amount of research has focused on the mechanisms of acute lung injury and yet the exact sequence of events and media tors in inflammatory cascade, which result in acute respiratory failure from ARDS, is not known but many possibilities exist. The definition of ARDS has been gradua11y modified in recent years and investigators around the world are now co11aborating in order to establish more uniform concepts in identification, risk factors and mechanisms of lung injury, which someday will result in improved approaches to management. Already, at least some centers are showing improved outcomes in ARDS, achieving an approximate 60% survival rate. In the past, most large series documented only about a 40% survivability taking a11 causes of ARDS. This apparent progress is likely attributable to more meticulous and disciplined care than any specific pharmacologic attack on the basic mechanism resulting in ARDS.

Whereas a great deal has been learned during the past quarter century about the inflammatory processes associated with sepsis (and other related conditions, such as ischemia/reperfusion injury), our understanding is far less developed with respect to the pathophysiological events that lead to organ dysfunction under these conditions.

The pathophysiology of sepsis can be regarded as a series of steps, beginning with the invasion of normally sterile tissue by microbes and the elaboration of various pro-inflammatory mediators. The final common pathway is often the development of the multiple organ dysfunction syndrome (MODS). Whereas a great deal has been learned during the past quarter century about the inflammatory processes associated with sepsis (and other related conditions, such as ischemia/reperfusion injury), our understanding is far less developed with respect to the pathophysiological events that lead to organ dysfunction under these conditions. Nevertheless, efforts by both clinical and laboratory scientists are leading to new knowledge in this area. The chapters in this volume provide a state-of-the-art overview of many aspects of the pathophysiology of organ dysfunction in critical illness.

The pathophysiology of sepsis can be regarded as a series of steps, beginning with the invasion of normally sterile tissue by microbes and the elaboration of various pro-inflammatory mediators. The final common pathway is often the development of the multiple organ dysfunction syndrome (MODS). Whereas a great deal has been learned during the past quarter century about the inflammatory processes associated with sepsis (and other related conditions, such as ischemia/reperfusion injury), our understanding is far less developed with respect to the pathophysiological events that lead to organ dysfunction under these conditions. Nevertheless, efforts by both clinical and laboratory scientists are leading to new knowledge in this area. The chapters in this volume provide a state-of-the-art overview of many aspects of the pathophysiology of organ dysfunction in critical illness.

To integrate current knowledge in terms of basic and clinical science and to highlight problems, thirty world-renowned experts in the field of acute lung injury describe the state of up to date knowledge regarding the epidemiology, pathophysiology, and clinical management of acute lung injury. Novel techniques for the clinical support of these difficult patients are discussed in full. Prospects for successful pharmacological intervention are also outlined. This book is aimed at those practising within the field of critical care and is likely to become an indispensable aid to all concerned with the investigation and management of patients with severe respiratory failure.