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Review
. 2017 Jan;33(1):167-191.
doi: 10.1016/j.ccc.2016.08.006.

Postinjury Inflammation and Organ Dysfunction

Angela Sauaia  1 , Frederick A Moore  2 , Ernest E Moore  3
Affiliations
Review

Postinjury Inflammation and Organ Dysfunction

Angela Sauaia et al. Crit Care Clin. 2017 Jan.

Abstract

The development of organ dysfunction (OD) is related to the intensity and balance between trauma-induced simultaneous, opposite inflammatory responses. Early proinflammation via innate immune system activation may cause early OD, whereas antiinflammation, via inhibition of the adaptive immune system and apoptosis, may induce immunoparalysis, impaired healing, infections, and late OD. Patients discharged with low-level OD may develop the persistent inflammation-immunosuppression catabolism syndrome. Although the incidence of multiple organ failure has decreased over time, it remains morbid, lethal, and resource intensive. However, single OD, especially acute lung injury, remains frequent. Treatment is limited, and prevention remains the mainstay strategy.

Keywords: CARS; Organ dysfunction; PICS; Postinjury inflammation; SARS; SIRS.

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Figures

Figure 1
Figure 1
Theoretical framework for postinjury multiple organ failure: The synchronous immunoinflammatory model
Figure 2
Figure 2. Kaplan-Meyer curves for MOF incidence and outcomes across biennial periods from 2003–2010 in 1643 adult, blunt trauma patients admitted to four US trauma centers (Glue Grant Dataset)
*stratum 2004=2003–2004; stratum 2006=2005–2006; stratum 2008=2007–2008; stratum=2009–2010
Figure 3
Figure 3
MOF onset and respective case-fatality rates
Figure 4
Figure 4
Response to trauma: hemostatic, inflammatory, endocrine and neurological systems interaction
See this image and copyright information in PMC

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MeSH terms