Management of the acute respiratory distress syndrome.
Significant advances have occurred in the knowledge of the pathogenesis of ARDS. It is now recognized that ARDS is a manifestation of a diffuse process that results from a complicated cascade of events following an initial insult or injury. Mechanical ventilation and PEEP are still important components of supportive therapy. To avoid ventilator-associated lung injury there is emphasis on targeting ventilator management based on measurement of pulmonary mechanics. For those with resistant hypoxia and severe pulmonary hypertension adjunctive modalities, such as prone positioning and low-dose iNO, may provide important benefit. Alternative modes of supporting gas exchange, such as with partial liquid ventilation and extracorporeal gas-exchange, may serve as rescue therapies. Advances in cell and molecular biology have contributed to a better understanding of the role of inflammatory cells and mediators that contribute to the acute lung injury and the pathophysiology of the syndrome that manifests as ARDS. Based on this new understanding, the potential targets for intervention to ameliorate the systemic inflammatory response have proliferated. Examples include the cytokine network and its receptors, antioxidants, and endothelins. Apart from the challenge of testing these agents in experimental models, it seems likely that determination of the optimum combination of agents will become an equally important endeavor. A particular challenge is to develop better methods of predicting which of the many at-risk patients will go on to full-blown ARDS and MODS, thereby targeting subgroups of patients most likely to benefit from anti-inflammatory therapies. Similarly, the adverse effects of immunosuppressive therapy may be diminished by improved, perhaps molecular, techniques to detect microbial pathogens and permit differentiation between Systemic inflammatory response syndrome and sepsis.
Departments of Medicine and Emergency Medicine, Critical Care Service, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71103-4228, USA. sconrad@lsuhsc.edu
Steven A
SA
Conrad
Akhil
A
Bidani
D000818:Animals; D002986:Clinical Trials as Topic; D015199:Extracorporeal Membrane Oxygenation / Q000379:methods; D006801:Humans; D009466:Neuromuscular Blocking Agents / Q000627:therapeutic use; D009569:Nitric Oxide / Q000627:therapeutic use; D011175:Positive-Pressure Respiration; D016684:Prone Position / Q000502:physiology; D011659:Pulmonary Gas Exchange / Q000502:physiology; D012121:Respiration, Artificial / Q000009:adverse effects; D012128:Respiratory Distress Syndrome / Q000503:physiopathology / Q000628:therapy*; D015656:Respiratory Mechanics / Q000502:physiology; D014665:Vasodilator Agents / Q000627:therapeutic use; D014882:Water-Electrolyte Balance / Q000502:physiology
D009466:Neuromuscular Blocking Agents; D014665:Vasodilator Agents; D009569:Nitric Oxide