Elsevier

Surgery

Volume 140, Issue 4, October 2006, Pages 640-648
Surgery

Central Surgical Association
Decreased progression of postinjury lung dysfunction to the acute respiratory distress syndrome and multiple organ failure

Presented at the 63rd Annual Meeting of the Central Surgical Association, Louisville, Kentucky, March 9-11, 2006.
https://doi.org/10.1016/j.surg.2006.06.015Get rights and content

Background

Postinjury organ dysfunction is a result of unbridled systemic hyperinflammation. According to the two-event construct, patients are resuscitated into an early vulnerable window of systemic hyperinflammation (primed) in which a second otherwise innocuous event precipitates uncontrolled hyperinflammation, leading to secondary organ damage and dysfunction (activated). Recent efforts to decrease postinjury morbidity have focused on limiting the potential of second events and systemic inflammation. We hypothesized that the collective effects of recently implemented therapeutic strategies have resulted in decreased activation of the systemic inflammatory response relative to priming in recent years.

Methods

Data were collected prospectively on trauma patients at risk for postinjury multiple organ failure (MOF). Inclusion criteria were age >15 years, trauma intensive care unit admission, Injury Severity Score >15 and survival >48 hours. Isolated head injuries and head injuries with an extracranial abbreviated injury score <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 with the use of the Denver MOF Scale. Acute respiratory distress syndrome (ARDS) was defined according to the consensus definition.

Results

Over a 6.5-year period 897 patients were studied; 271 (31%) developed ARDS, and 226 (25%) developed MOF. Early lung dysfunction, as a measure of systemic priming, did not change over the study period. In contrast, the incidence of ARDS and MOF decreased from 43% to 25% and 33% to 12%, respectively. The incidence of early MOF decreased from 22% to 7% over the study period.

Conclusions

Priming of the postinjury inflammatory response is an early event and is primarily influenced by the injury itself. Recent advances in postinjury care such as judicious blood transfusion, lung protective ventilation, treatment of adrenal insufficiency, and tight glucose control are known to attenuate systemic inflammation. Step-wise adoption of these therapies is coincident with a decrease in the destructive processes resulting in ARDS and MOF. The global effect is a decrease in activation of the systemic inflammatory response over recent years.

Section snippets

Methods

Trauma patients admitted to the Rocky Mountain Regional Trauma Center surgical intensive care unit (SICU) at Denver Health Medical Center (DHMC) were studied prospectively from 1992 until June 30, 2004. DHMC is a state designated Level I trauma center verified by the American College of Surgeons Committee on Trauma. Inclusion criteria were Injury Severity Score (ISS) greater than 15, survival longer than 48 hours from injury, admission to the SICU within 24 hours of injury, and age greater than

Results

Data were collected on 1415 severely injured patients over a 12.5-year period ending June 2004. Patient data collected before 1997 was excluded in this study since, at that time, the data collection process was revised, and a more complete and homogeneous data set was collected thereafter. The present study included data on 897 patients collected since January 1, 1997. The majority (640 [71%]) were male with a mean ± SD age of 38.4 ± 17.1 years. Blunt, penetrating, and mixed mechanisms

Discussion

In 1977 Eiseman7 described MOF in 42 critically ill surgical patients. A period of intense clinical investigation followed in which the definition of postinjury MOF was refined and its risk factors identified.4, 8, 9 Several authors recognized the pivotal role of the immune system in causing postinjury secondary organ dysfunction.10, 11, 12, 13, 14 The focus of study then shifted in the 1990s to uncovering the pathophysiology responsible for this syndrome. Initially thought to be a result of

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    Supported in part by National Institutes of Health (NIH) grants P50GM49222, T32GM08315, U546M62119, and the Jourdan Block Trauma Foundation.

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