Epidemiology of trauma deaths: a reassessment.

St. Anthony's Hospital, St. Petersburg, Florida, United States
The Journal of trauma (Impact Factor: 2.96). 03/1995; 38(2):185-93. DOI: 10.1097/00005373-199307000-00073
Source: PubMed

ABSTRACT Recognizing the impact of the 1977 San Francisco study of trauma deaths in trauma care, our purpose was to reassess those findings in a contemporary trauma system.
All trauma deaths occurring in Denver City and County during 1992 were reviewed; data were obtained by cross-referencing four databases: paramedic trip reports, trauma registries, coroner autopsy reports and police reports.
There were 289 postinjury fatalities; mean age was 36.8 +/- 1.2 years and mean Injury Severity Score (ISS) was 35.7 +/- 1.2. Predominant injury mechanisms were gunshot wounds in 121 (42%), motorvehicle accidents in 75 (38%) and falls in 23 (8%) cases. Seven (2%) individuals sustained lethal burns. Ninety eight (34%) deaths occurred in the pre-hospital setting. The remaining 191 (66%) patients were transported to the hospital. Of these, 154 (81%) died in the first 48 hours (acute), 11 (6%) within three to seven days (early) and 26 (14%) after seven days (late). Central nervous system injuries were the most frequent cause of death (42%), followed by exsanguination (39%) and organ failure (7%). While acute and early deaths were mostly due to the first two causes, organ failure was the most common cause of late death (61%).
In comparison with the previous report, we observed similar injury mechanisms, demographics and causes of death. However, in our experience, there was an improved access to the medical system, greater proportion of late deaths due to brain injury and lack of the classic trimodal distribution.

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    ABSTRACT: Stress hyperglycemia following trauma has been shown to potentiate morbidity and mortality. Glucose control in obese patients can be challenging due to insulin resistance. Thus, understanding the mechanisms for glucose generation following hemorrhage may provide important insights into alternative options for glycemic control in obesity. Obesity is characterized by elevated glycogen and increased hepatic β2-adrenergic activity, which play major roles in glucose production after hemorrhage. We hypothesized that, in obesity, hepatic glycogenolysis is enhanced during stress hyperglycemia due to increased hepatic β2-adrenoceptor activation. Hemorrhage was performed in conscious lean Zucker (LZ) and obese Zucker rats (OZ) by withdrawing 35% total blood volume over 10 min. Liver glycogen content and plasma levels of glucose, insulin, and glucagon were measured before and 1 h after hemorrhage. The hyperglycemic response was greater in OZ as compared to LZ, but glycogen content was similarly reduced in both groups. Subsequently, OZ had a greater fall in insulin compared to LZ. Glucagon levels were significantly increased 1 h after hemorrhage in LZ but not in OZ. To test the direct adrenergic effects on the liver after hemorrhage, we treated animals before hemorrhage with a selective β2-adrenoceptor antagonist, ICI-118,551 (ICI; 2 mg/kg/h, i.v.). After hemorrhage, ICI significantly reduced hyperglycemia in both LZ and OZ, independent of hormonal changes, but there was a significantly decreased hepatic glycogenolysis in OZ. These results suggest that the hemorrhage-induced hepatic glycogenolysis is likely glucagon-dependent in LZ, whereas the β2-adrenoceptor plays a greater role in OZ. © 2014 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.
    12/2014; 2(12). DOI:10.14814/phy2.12215
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    ABSTRACT: Newer studies have hypothesised about a coagulopathy that occurs early after trauma, early trauma induced coagulopathy, ETIC, and is defined by an elevated admission prothrombin time (PT). Also, referred to by some authors as acute traumatic coagulopathy, it has been most often studied in cohorts of severely injured or hypotensive patients. However, we wanted to prospectively investigate ETIC in a large all-comers cohort to confirm its prevalence across the entire spectrum of injury, to evaluate its risk pattern and to determine a possible relationship to reduced survival. We conducted a prospective cohort study at a Level I trauma centre from July 15, 2008 to November 15, 2009. Demographics, injury mechanism, time from injury and to hospital arrival, fluid and blood administration and vital signs were collected at hospital arrival and to the time of first blood sample collection for all patients admitted for 24h or longer. Our primary outcome was the incidence of mortality by the 28th hospital day, referred to as 28 day in-hospital mortality. 701 patients were included in the final study cohort. There was 75.3% male, 25.7% penetrating, with a mean age of 39 years. The overall mortality was 7.3%. ETIC occurred in 114 patients (16.3%) and was found to be independently associated with death (odds of death (per 0.10s increase in PT): 1.10, p=0.001). ETIC patients, as a group, were more severely injured, had more hypotension and head injury and used more crystalloid and blood products than non-ETIC patients. However, even mildly injured patients, who had an ISS<16, normal RTS score, and no fluid resuscitation, had an ETIC prevalence of 11.7% (11/94). ETIC is an early, primary post-injury coagulopathy that occurs in 16.3% of admitted trauma patients. It is associated with an increase in mortality, even when controlling for crystalloids, vital signs, injury severity and head injury. It can also be found in approximately 11% of mildly injured patients (patients without physiological derangement or blood product administration). Therefore, further elucidation of ETIC is strategic to impacting trauma patient outcome.
    Injury 11/2013; 45(5). DOI:10.1016/j.injury.2013.11.004 · 2.46 Impact Factor
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    ABSTRACT: AIMS: Trauma/Hemorrhagic shock (T/HS) induced gut injury is known to initiate a systemic inflammatory response which can lead to secondary lung injury. We have shown that vagal nerve stimulation (VNS) protects intestinal epithelial integrity after a severe burn insult. We hypothesize that VNS will protect the lung from injury following T/HS by preventing intestinal barrier failure. MAIN METHODS: Male Balb/c mice were subjected to a T/HS model with and without cervical VNS. Intestinal injury was evaluated by measuring changes in gut barrier function and tight junction protein localization. Lung injury was evaluated using histology and markers of lung inflammation. Using NF-kB-luciferase (NF-kB-luc) transgenic mice, NF-kb-DNA binding was measured by photon emission analysis at 4hrs after injury. KEY FINDINGS: T/HS is associated gut injury characterized by histologic injury, increased epithelial permeability, and altered localization of gut tight junction proteins. Cervical VNS prevented the T/HS-induced changes in gut barrier integrity. Gut injury after T/HS was associated with acute lung injury at 24 hours characterized by histologic injury, increased number of MPO positive stained cells and MPO enzymatic activity, and increased ICAM-1 expression in lung endothelium. VNS decreased T/HS-induced lung injury with a marked decrease in lung inflammation compared to T/HS alone. Lungs harvested from NF-kB-luc mice at 4hrs post VNS+T/HS demonstrated decreased DNA binding of NF-kB compared to T/HS alone as measured by changes in bioluminescence. SIGNIFICANCE: VNS is effective in protecting against acute lung injury caused by hemorrhagic shock through its ability to prevent gut barrier dysfunction.
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