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Acute respiratory distress syndrome and acute lung injury

Acute respiratory distress syndrome and acute lung injury
Acute respiratory distress syndrome and acute lung injury
Acute respiratory distress syndrome (ARDS) is a life threatening respiratory failure due to lung injury from a variety of precipitants. Pathologically ARDS is characterised by diffuse alveolar damage, alveolar capillary leakage, and protein rich pulmonary oedema leading to the clinical manifestation of poor lung compliance, severe hypoxaemia, and bilateral infiltrates on chest radiograph. Several aetiological factors associated with the development of ARDS are identified with sepsis, pneumonia, and trauma with multiple transfusions accounting for most cases. Despite the absence of a robust diagnostic definition, extensive epidemiological investigations suggest ARDS remains a significant health burden with substantial morbidity and mortality. Improvements in outcome following ARDS over the past decade are in part due to improved strategies of mechanical ventilation and advanced support of other failing organs. Optimal treatment involves judicious fluid management, protective lung ventilation with low tidal volumes and moderate positive end expiratory pressure, multi-organ support, and treatment where possible of the underlying cause. Moreover, advances in general supportive measures such as appropriate antimicrobial therapy, early enteral nutrition, prophylaxis against venous thromboembolism and gastrointestinal ulceration are likely contributory reasons for the improved outcomes. Although therapies such as corticosteroids, nitric oxide, prostacyclins, exogenous surfactants, ketoconazole and antioxidants have shown promising clinical effects in animal models, these have failed to translate positively in human studies. Most recently, clinical trials with ?2 agonists aiding alveolar fluid clearance and immunonutrition with omega-3 fatty acids have also provided disappointing results. Despite these negative studies, mortality seems to be in decline due to advances in overall patient care. Future directions of research are likely to concentrate on identifying potential biomarkers or genetic markers to facilitate diagnosis, with phenotyping of patients to predict outcome and treatment response. Pharmacotherapies remain experimental and recent advances in the modulation of inflammation and novel cellular based therapies, such as mesenchymal stem cells, may reduce lung injury and facilitate repair.
0032-5473
612-622
Dushianthan, A.
bbc28c98-a128-40f0-bfa9-2669740687cf
Grocott, M.P.W.
1e87b741-513e-4a22-be13-0f7bb344e8c2
Postle, A.D.
0fa17988-b4a0-4cdc-819a-9ae15c5dad66
Cusack, R.
ed7872ed-eeea-4d95-9105-f32622b6d8d3
Dushianthan, A.
bbc28c98-a128-40f0-bfa9-2669740687cf
Grocott, M.P.W.
1e87b741-513e-4a22-be13-0f7bb344e8c2
Postle, A.D.
0fa17988-b4a0-4cdc-819a-9ae15c5dad66
Cusack, R.
ed7872ed-eeea-4d95-9105-f32622b6d8d3

Dushianthan, A., Grocott, M.P.W., Postle, A.D. and Cusack, R. (2011) Acute respiratory distress syndrome and acute lung injury. Postgraduate Medical Journal, 87 (1031), 612-622. (doi:10.1136/pgmj.2011.118398). (PMID:21642654)

Record type: Article

Abstract

Acute respiratory distress syndrome (ARDS) is a life threatening respiratory failure due to lung injury from a variety of precipitants. Pathologically ARDS is characterised by diffuse alveolar damage, alveolar capillary leakage, and protein rich pulmonary oedema leading to the clinical manifestation of poor lung compliance, severe hypoxaemia, and bilateral infiltrates on chest radiograph. Several aetiological factors associated with the development of ARDS are identified with sepsis, pneumonia, and trauma with multiple transfusions accounting for most cases. Despite the absence of a robust diagnostic definition, extensive epidemiological investigations suggest ARDS remains a significant health burden with substantial morbidity and mortality. Improvements in outcome following ARDS over the past decade are in part due to improved strategies of mechanical ventilation and advanced support of other failing organs. Optimal treatment involves judicious fluid management, protective lung ventilation with low tidal volumes and moderate positive end expiratory pressure, multi-organ support, and treatment where possible of the underlying cause. Moreover, advances in general supportive measures such as appropriate antimicrobial therapy, early enteral nutrition, prophylaxis against venous thromboembolism and gastrointestinal ulceration are likely contributory reasons for the improved outcomes. Although therapies such as corticosteroids, nitric oxide, prostacyclins, exogenous surfactants, ketoconazole and antioxidants have shown promising clinical effects in animal models, these have failed to translate positively in human studies. Most recently, clinical trials with ?2 agonists aiding alveolar fluid clearance and immunonutrition with omega-3 fatty acids have also provided disappointing results. Despite these negative studies, mortality seems to be in decline due to advances in overall patient care. Future directions of research are likely to concentrate on identifying potential biomarkers or genetic markers to facilitate diagnosis, with phenotyping of patients to predict outcome and treatment response. Pharmacotherapies remain experimental and recent advances in the modulation of inflammation and novel cellular based therapies, such as mesenchymal stem cells, may reduce lung injury and facilitate repair.

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More information

e-pub ahead of print date: 4 June 2011
Published date: September 2011
Organisations: Clinical & Experimental Sciences

Identifiers

Local EPrints ID: 195521
URI: http://eprints.soton.ac.uk/id/eprint/195521
ISSN: 0032-5473
PURE UUID: c96dceb3-32f0-4cb2-99dc-193e18545696
ORCID for M.P.W. Grocott: ORCID iD orcid.org/0000-0002-9484-7581
ORCID for A.D. Postle: ORCID iD orcid.org/0000-0001-7361-0756

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Date deposited: 22 Aug 2011 15:32
Last modified: 15 Mar 2024 03:33

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Contributors

Author: A. Dushianthan
Author: M.P.W. Grocott ORCID iD
Author: A.D. Postle ORCID iD
Author: R. Cusack

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