ATS/ERS statement: raised volume forced expirations in infants: guidelines for current practice.
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Biomedical subjects
Publications and source records attributed to European Respiratory Society.
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OBJECTIVE: The purpose of the conference was to provide clinical practice guidance in end-of-life care in the ICU via answers to previously identified questions relating to variability in practice, inadequate predictive models for death, elusive knowledge of patient preferences, poor communication between staff and surrogates, insufficient or absent training of healthcare providers, the use of imprecise and insensitive terminology and incomplete documentation in the medical record. PARTICIPANTS: Presenters and jury were selected by the sponsoring organizations (American Thoracic Society, European Respiratory Society, European Society of Intensive Care Medicine, Society of Critical Care Medicine, Société de Réanimation de Langue Française). Presenters were experts on the question they addressed. Jury members were general intensivists without special expertise in the areas considered. Experts presented in an open session to jurors and other healthcare professionals. EVIDENCE: Experts prepared review papers on their specific topics in advance of the conference for the jury's reference in developing the consensus statement. CONSENSUS PROCESS: Jurors heard experts' presentations over 2 days and asked questions of the experts during the open sessions. Jury deliberation with access to the review papers occurred for 2 days following the conference. A writing committee drafted the consensus statement for review by the entire jury. The 5 sponsoring organizations reviewed the document and suggested revisions to be incorporated into the final statement. CONCLUSIONS: Strong recommendations for research to improve end-of-life care were made. The jury advocates a shared approach to end-of-life decision-making involving the caregiver team and patient surrogates. Respect for patient autonomy and the intention to honor decisions to decline unwanted treatments should be conveyed to the family. The process is one of negotiation, and the outcome will be determined by the personalities and beliefs of the participants. Ultimately, it is the attending physician's responsibility, as leader of the team, to decide on the reasonableness of the planned action. If a conflict cannot be resolved, an ethics consultation may be helpful. The patient must be assured of a pain-free death. The jury subscribes to the moral and legal principles that prohibit administering treatments specifically designed to hasten death. The patient must be given sufficient analgesia to alleviate pain and distress; if such analgesia hastens death, this "double-effect" should not detract from the primary aim to ensure comfort.
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Idiopathic pulmonary fibrosis is a progressive and usually fatal lung disease characterized by fibroblast proliferation and extracellular matrix remodeling, which result in irreversible distortion of the lung's architecture. Although the pathogenetic mechanisms remain to be determined, the prevailing hypothesis holds that fibrosis is preceded and provoked by a chronic inflammatory process that injures the lung and modulates lung fibrogenesis, leading to the end-stage fibrotic scar. However, there is little evidence that inflammation is prominent in early disease, and it is unclear whether inflammation is relevant to the development of the fibrotic process. Evidence suggests that inflammation does not play a pivotal role. Inflammation is not a prominent histopathologic finding, and epithelial injury in the absence of ongoing inflammation is sufficient to stimulate the development of fibrosis. In addition, the inflammatory response to a lung fibrogenic insult is not necessarily related to the fibrotic response. Clinical measurements of inflammation fail to correlate with stage or outcome, and potent anti-inflammatory therapy does not improve outcome. This review presents a growing body of evidence suggesting that idiopathic pulmonary fibrosis involves abnormal wound healing in response to multiple, microscopic sites of ongoing alveolar epithelial injury and activation associated with the formation of patchy fibroblast-myofibroblast foci, which evolve to fibrosis. Progress in understanding the fibrogenic mechanisms in the lung is likely to yield more effective therapies.