Postinjury Inflammation and Organ Dysfunction - 14/12/17

Doi : 10.1016/j.ccc.2016.08.006

Angela Sauaia, MD, PhD ^a,^⁎ , Frederick A. Moore, MD ^b, Ernest E. Moore, MD ^c
^a University of Colorado Denver, 655 Broadway #365, Denver, CO 80203, USA
^b University of Florida, PO BOX 100108, Gainesville, FL 32610, USA
^c Denver Health Medical Center, University of Colorado Denver, 655 Broadway #365, Denver, CO 80203, USA

^∗Corresponding author.

Résumé

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.

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Keywords : Organ dysfunction, Postinjury inflammation, SIRS, CARS, SARS, PICS

Plan

Disclosures: Drs A. Sauaia and E.E. Moore received funding from the National Institute of General Medical Sciences grant P50 GM049222 and the National Heart, Lung, and Blood Institute grant UM1 HL120877. Dr Frederick A. Moore received funding from the National Institute of General Medical Sciences grant P50 GM111152. The content of this article is solely the responsibility of the authors and does not necessarily represent the official views of the NIGMS, NHLBI, or National Institutes of Health. The authors have no commercial or financial conflicts of interest.