Literature DB >> 16269305

The role of the lung in postinjury multiple organ failure.

David J Ciesla1, Ernest E Moore, Jeffrey L Johnson, Jon M Burch, Clay C Cothren, Angela Sauaia.   

Abstract

BACKGROUND: Postinjury multiple organ failure (MOF) is a result of a dysfunctional inflammatory response to severe injury and shock. Acute lung injury is thought to promote further organ dysfunction by the systemic release of inflammatory mediators from injured lung tissue. Although clinical evidence supports this model, a clear understanding of the relationship between lung dysfunction and multiple organ failure has yet to be defined. We hypothesized that respiratory dysfunction is an early obligate event in the progression of postinjury MOF.
METHODS: Data were collected prospectively on 1,344 trauma patients at risk for postinjury MOF. Inclusion criteria were age greater than 16 years, trauma intensive care unit admission, Injury Severity Score greater than 15, and survival longer than 48 hours. Isolated head injuries and head injuries with an extracranial abbreviated injury score of less than 2 were excluded. Daily physiologic and laboratory data were collected through surgical intensive care unit day 28 and clinical events were recorded thereafter until death or hospital discharge. Organ failure was characterized using the Denver MOF scale.
RESULTS: Organ dysfunction was observed in 1,011 (75%) of 1,344 patients. Lung dysfunction was observed in 951 (94%) patients with 1 or more organ dysfunctions and 598 (99%) of 605 patients with 2 or more organ dysfunctions. Lung dysfunction preceded heart, liver, and kidney dysfunction by an average of 0.6 +/- 0.2 days, 4.8 +/- 0.2 days, and 5.5 +/- 0.5 days, respectively. The severity of lung dysfunction correlated with the severity of heart, liver, and kidney dysfunction, and the number of other dysfunctional organ systems.
CONCLUSIONS: Postinjury respiratory dysfunction is an obligate event that precedes heart, liver, and kidney failure. The severity of other organ dysfunction is related directly to the severity of respiratory dysfunction. These data implicate lung dysfunction as central to the promotion of pathogenic inflammation and the development of postinjury MOF.

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Year:  2005        PMID: 16269305     DOI: 10.1016/j.surg.2005.07.020

Source DB:  PubMed          Journal:  Surgery        ISSN: 0039-6060            Impact factor:   3.982


  52 in total

1.  Health care utilization and the cost of posttraumatic acute respiratory distress syndrome care.

Authors:  Anamaria J Robles; Lucy Z Kornblith; Carolyn M Hendrickson; Benjamin M Howard; Amanda S Conroy; Farzad Moazed; Carolyn S Calfee; Mitchell J Cohen; Rachael A Callcut
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2.  Platelet transfusion increases risk for acute respiratory distress syndrome in non-massively transfused blunt trauma patients.

Authors:  George Kasotakis; Nichole Starr; Erek Nelson; Bedabrata Sarkar; Peter Ashley Burke; Daniel George Remick; Ronald Gary Tompkins
Journal:  Eur J Trauma Emerg Surg       Date:  2018-04-07       Impact factor: 3.693

3.  Hypertonic saline inhibits arachidonic acid priming of the human neutrophil oxidase.

Authors:  Luis Lee; Marguerite R Kelher; Ernest E Moore; Anirban Banerjee; Christopher C Silliman
Journal:  J Surg Res       Date:  2011-07-14       Impact factor: 2.192

4.  Prevention of trauma/hemorrhagic shock-induced lung apoptosis by IL-6-mediated activation of Stat3.

Authors:  Ana Moran; Anna I Tsimelzon; Mary-Ann A Mastrangelo; Yong Wu; Bi Yu; Susan G Hilsenbeck; Valeria Poli; David J Tweardy
Journal:  Clin Transl Sci       Date:  2009-02       Impact factor: 4.689

5.  Nebulized hypertonic saline attenuates acute lung injury following trauma and hemorrhagic shock via inhibition of matrix metalloproteinase-13.

Authors:  Max Wohlauer; Ernest E Moore; Christopher C Silliman; Miguel Fragoso; Fabia Gamboni; Jeffrey Harr; Frank Accurso; Frank Wright; James Haenel; David Fullerton; Anirban Banerjee
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6.  Early lung ultrasonography predicts the occurrence of acute respiratory distress syndrome in blunt trauma patients.

Authors:  Damien Leblanc; Clément Bouvet; Franck Degiovanni; Cosmina Nedelcu; Guillaume Bouhours; Emmanuel Rineau; Catherine Ridereau-Zins; Laurent Beydon; Sigismond Lasocki
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7.  Ciglitazone, a novel inhibitor of lung apoptosis following hemorrhagic shock.

Authors:  Ranjit S Chima; Paul W Hake; Giovanna Piraino; Prajakta Mangeshkar; Michael O'Connor; Basilia Zingarelli
Journal:  Int J Clin Exp Med       Date:  2010-01-01

8.  Inhibition of NADPH oxidase prevents acute lung injury in obese rats following severe trauma.

Authors:  Lusha Xiang; Silu Lu; Peter N Mittwede; John S Clemmer; Robert L Hester
Journal:  Am J Physiol Heart Circ Physiol       Date:  2014-01-10       Impact factor: 4.733

9.  Prevention of trauma and hemorrhagic shock-mediated liver apoptosis by activation of stat3alpha.

Authors:  Ana Moran; Ayse Akcan Arikan; Mary-Ann A Mastrangelo; Yong Wu; Bi Yu; Valeria Poli; David J Tweardy
Journal:  Int J Clin Exp Med       Date:  2008-06-15

10.  Ciglitazone ameliorates lung inflammation by modulating the inhibitor kappaB protein kinase/nuclear factor-kappaB pathway after hemorrhagic shock.

Authors:  Ranjit S Chima; Paul W Hake; Giovanna Piraino; Prajakta Mangeshkar; Alvin Denenberg; Basilia Zingarelli
Journal:  Crit Care Med       Date:  2008-10       Impact factor: 7.598

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