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World J Surg (2010) 34:158–163 DOI 10.1007/s00268-009-0266-1

Epidemiology of Traumatic Deaths: Comprehensive Population-Based Assessment Julie A. Evans • Karlijn J. P. van Wessem • Debra McDougall • Kevin A. Lee • Timothy Lyons Zsolt J. Balogh



Published online: 31 October 2009 Ó Socie´te´ Internationale de Chirurgie 2009

Abstract Background The epidemiology of traumatic deaths was periodically described during the development of the American trauma system between 1977 and 1995. Recognizing the impact of aging populations and the potential changes in injury mechanisms, the purpose of this work was to provide a comprehensive, prospective, populationbased study of Australian trauma-related deaths and compare the results with those of landmark studies. Methods All prehospitalization and in-hospital trauma deaths occurring in an inclusive trauma system at a single Level 1 trauma center [400 patients with an injury severity score (ISS) [15/year] underwent autopsy and were prospectively evaluated during 2005. High-energy (HE) and low-energy (LE) deaths were categorized based on the mechanism of the injury, time frame (prehospitalization, \48 hours, 2–7 days, [7 days), and cause [which was determined by an expert panel and included central nervous system-related (CNS), exsanguination, CNS ? exsanguination, airway, multiple organ failure (MOF)]. Data are presented as a percent or the mean ± SEM. Results There were 175 deaths during the 12-month period. For the 103 HE fatalities (age 43 ± 2 years, ISS 49 ± 2, male 63%), the predominant mechanisms were motor vehicle related (72%), falls (4%), gunshots (8%),

J. A. Evans  K. J. P. van Wessem  D. McDougall  Z. J. Balogh (&) Department of Traumatology, Division of Surgery, John Hunter Hospital and University of Newcastle, Locked Bag 1, Hunter Region Mail Centre, Newcastle, NSW 2310, Australia e-mail: [email protected] K. A. Lee  T. Lyons Department of Forensic Medicine, John Hunter Hospital and University of Newcastle, Newcastle, NSW 2310, Australia

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stabs (6%), and burns (5%). In all, 66% of the patients died during the prehospital phase, 27% died after \48 hours in hospital, 5% died after 3 to 7 days in hospital, and 2% died after [7 days. CNS (33%) and exsanguination (33%) were the most common causes of deaths, followed by CNS ? exsanguination (17%) and airway compromise 8%; MOF occurred in only 3%. Six percent of the deaths were undetermined. All LE deaths (n = 72, age 83 ± 1 years, ISS 14 ± 1, male 45%) were due to low falls. All LE patients died in hospital (20%\48 hours, 32% after 3–7 days, 48% after 7 days). The causes of deaths were head injury (26%) and complications of skeletal injuries (74%). Conclusions The HE injury mechanisms, time frames, and causes in our study are different from those in the earlier, seminal reports. The classic trimodal death distribution is much more skewed to early death. Exsanguination became as frequent as lethal head injuries, but the incidence of fatal MOF is lower than reported earlier. LE trauma is responsible for 41% of the postinjury mortality, with distinct epidemiology. The LE group deserves more attention and further investigation.

Introduction In 1977, Baker et al. conducted a study on trauma deaths in the San Francisco area over a 1-year period describing the classic trimodal distribution of trauma deaths [1]. The first peak included immediate deaths, primarily the result of nonsurvivable central nervous system (CNS) injury and rapid exsanguination. The second peak included the early hospital deaths, also mainly caused by brain injury and exsanguination. The third peak included the late deaths, 75% of which were attributed to multiple organ failure (MOF). Ten years later Shackford et al. showed that injury

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continued to account for an enormous loss of life despite improvements in survival by trauma systems based on this population-based study [2]. In 1992, Sauaia et al. reassessed the study done by Baker’s group. They concluded that there was no longer a trimodal distribution and that the observed shift from the prehospital deaths toward early (0–48 hours) hospital deaths could be attributed to better prehospital care [3]. Most of the Australian studies have either focused on prehospital [4] or hospital [5–7] mortalities only. To date, there is no comprehensive population-based Australian study describing both prehospital and in-hospital trauma deaths. Recognizing the impact of aging populations and the potential changes in injury mechanisms, the purpose of this work was to provide a comprehensive, prospective, population-based study of Australian trauma-related deaths and compare the results with those of landmark studies.

Materials and methods The studied area, the Hunter New England region, is located in New South Wales (NSW) in Australia. The Hunter New England area is 130,000 square kilometers and has a rural and metropolitan mixed population of 840,000. The study was conducted at John Hunter Hospital, a statedesignated, Royal Australasian College of Surgeons-verified Level 1 trauma center, the only major tertiary referral hospital for the region. In Australia, the Advanced Trauma Life Support course is compulsory for all surgical trainees, and the trauma verification process is similar to the one developed by the Committee on Trauma of the American College of Surgeons. Prehospital care in the Hunter region is provided by the Ambulance Service of NSW and utilizes both road and helicopter primary retrieval from the trauma scene. By protocol, all major trauma patients in the Hunter region are transported to the Level 1 trauma center. The Hunter New England Area Health Ethics Committee (‘‘IRB’’) approved this prospective population-based epidemiologic study. Autopsies and medical records on all traumatic deaths occurring in the Hunter region from February 1, 2005 to January 31, 2006 were reviewed prospectively. Deaths related to electrocution, drowning, hanging asphyxiation, strangling, and poisoning were excluded from the data analysis. Traumatic deaths were categorized as either lowenergy (LE) or high-energy (HE) trauma. HE trauma included falls of [3 meters, road and traffic-related injuries, industrial injuries, major burns, and trauma related to gunshot and stab wounds. All HE deaths were subjected to a forensic autopsy conducted at the Newcastle Department of Forensic Medicine. The forensic autopsies and medical

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records were examined, and an expert panel defined the cause of death. Deaths were categorized based on mechanism, time frame (prehospital, \48 hours, 2–7 days, and [7 days after the injury) and causes (predominantly CNS-related injury, exsanguination from uncontrolled bleeding, CNS ? exsanguination, airway compromise, MOF). This classification is identical to the categories used in one of the previous studies [3]. Data are presented as a percent or the mean ± SEM.

Results During the 12-month study period 175 patients died. The mean age in the entire group was 55 ± 4 years, with an injury severity score (ISS) of 36 ± 4. In all, 55% of the group were male. A total of 103 of these 175 fatalities (59%) sustained HE trauma. The mean ISS in this HE trauma group was 49 ± 2. The mean age was 43 ± 2 years, and 63% of the patients were male. Altogether, 72 of the 175 deaths (41%) were due to LE trauma. The mean ISS in this group was 14 ± 1. Their mean age was 83 ± 1 years, and 45% were male. In all, 41% of the overall fatalities were caused by LE trauma (Table 1). In our study 12.3 per 100,000 people died of HE trauma, whereas LE trauma caused 8.6 deaths per 100,000 per year. In total, 20.8 per 100,000 people died from injuries caused by trauma. The predominant mechanisms of HE trauma were roadand motor vehicle-related (72%), falls [3 meters (4%), gunshots (8%), stabs (6%), and burns (5%). Altogether 66% of the HE deaths occurred before hospitalization, 27% within 48 hours of hospital admission, 5% after 3 to 7 days, and 2% after [7 days (Fig. 1). The CNS-related injuries (33%) and exsanguination (33%) were the most common causes of death followed by CNS ? exsanguination (17%) and airway compromise (8%); MOF occurred in only 3%. Six percent of the deaths were undetermined (Fig. 2). Table 1 Demographics and injury severity of the traumatic deaths Parameter

Total

High-energy injury

Low-energy injury

Patient factors No.

175 (100%)

103 (59%)

72 (41%)

Age (years)

55 ± 4

43 ± 2

83 ± 1

Male

55%

63%

45%

36 ± 4

49 ± 2

14 ± 1

ISS

ISS injury severity score

123

160

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% of traumatic deaths

The patients who died before hospitalization had an ISS of 58 ± 2 compared to an ISS of 45 ± 3 in patients who died in hospital within 48 hours. The patients who died after 48 hours had an ISS of 28 ± 2. The sources of exsanguination were traumatic aortic injury in 23%, chest injury (heart and pulmonary hilum) in 23%, and pelvic injury in 23%. In 14% the abdomen was 70 60 50 40 30 20 10 0 Prehospital

0-48 hours

2-7 days

>7 days

Newcastle 2005

Fig. 1 Time distribution of high-energy traumatic deaths (% of traumatic deaths)

the source of exsanguination, in 7% extremities was the source, and in 10% there was a combination of sources. The comparison of our results with previous landmark epidemiologic studies is depicted on Figs. 3, 4, 5, 6, 7, 8. The incidence of traumatic deaths has gradually decreased during the last three decades (Fig. 3). The relative percentage of prehospital deaths is higher in our study, but late hospital deaths had become rare (Fig. 4). Although the mean age of patients with traumatic death is steadily increasing (Fig. 5), the injury severity of the fatalities remained unchanged (Fig. 6). The comparison of causes of deaths showed that the relative frequency of mortality caused by bleeding is increasing as the ratio of CNS/ hemorrhage-related deaths is decreasing (Fig. 7). Deaths caused by MOF are less frequent in our cohort than in previous assessments (Fig. 8). All patients sustaining LE trauma had a fall of\1 meter. The time frames for the LE deaths are different from those for the HE deaths: None of the patients died prior to arrival to the hospital, 20% died within 48 hours of admission to the hospital, 31% died between 2 and 7 days after arrival, and 49% died after 7 days of hospitalization. The cause of

35 30

70

25

60

% of deaths

20 15 10 5

50 40 30 20

O F

in ed

10

Un de te rm

M

ay Ai rw

S+ Bl ee di ng

CN

Bl ee di ng

CN

S

0

0

Prehospital

0-48 hours

San Francisco 1977

Fig. 2 Causes of high-energy traumatic deaths (% of the total). CNS central nervous system injury-related deaths, MOF multiple organ failure

Fig. 3 Trends in the incidence of high-energy traumatic deaths, by city

San Diego 1987

2-7 days

>7 days

Denver 1992

Newcastle 2005

Fig. 4 Changing pattern of the time distribution of high-energy traumatic deaths

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deaths per 100,000

30 25 20 15 10 5 0 San Francisco 1977

123

San Diego 1987

Denver 1992

Newcastle 2005

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Fig. 5 Mean age of patients with high-energy traumatic death

50

Mean Age (years)

40

30

20

10

0 San Francisco 1977

Fig. 6 Injury severity score of the high-energy trauma death populations, by city and year

San Diego 1987

Denver 1992

Los Angeles 2002

Newcastle 2005

75

Injury Severity Score

60 30%

42%

14%

Penetrating Trauma

San Diego 1987

Denver 1992

Newcastle 2005

45

30

15

0

12

CNS / Bleeding

1.5

1.39 1.27 1

1

0.5

0 San Francisco 1977

San Diego 1987

Denver 1992

Newcastle 2005

Fig. 7 Change in the relative frequency of head injury- and hemorrhage-related deaths

LE deaths was a CNS injury in 74% and a complication after a skeletal injury in 26%. This study was designed to describe the populationbased epidemiology of trauma-related deaths—not to define the preventability of the deaths. The departmental mortality and morbidity data were retrospectively

% of Deaths caused by MOF

1.61

10 10 8

6.8

7

6 4

3

2 0 San Francisco 1977

San Diego 1987

Denver 1992

Newcastle 2005

Fig. 8 Relative incidence of multiple organ failure among traumatic deaths

cross-matched with our prospective database. This review showed that in the HE group one death was preventable and two were potentially preventable. In the LE group, one death was preventable and three were potentially preventable.

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Discussion The trimodal distribution of trauma deaths described during the 1980s is no longer applicable. Sauaia et al. showed that the number of prehospitalization deaths decreased and the number of patients who died between arrival at the hospital and 48 hours increased [3]. In our study we found that 66% of the HE trauma patients died prior to arrival at the hospital. Most of these patients bled to death from nonsurvivable injuries. Other authors [2, 3, 7] have also demonstrated this relative increase in early prehospitalization deaths. When our results were compared to those of previous studies [1–3], we found fewer deaths per 100,000 than were cited in the studies during the 1970s and 1980s (Fig. 3). Our rate is also lower than earlier published data from the Department of Human Services and Health (DHSH) in Australia. According to the DHSH, 23 per 100,000 people in Australia die from transport-related injuries, and falls and trauma are the major causes of death in people \44 years of age [8]. This decline in traumatic deaths is likely to be attributed to the improved care for trauma patients over the last 30 years, which was confirmed by a recent study by Cothren et al., who reassessed the trauma mortality in Denver, Colorado (USA) 10 years after their first study [3, 9]. However, when the time frames in which the patients die are compared, not much difference is seen between the study performed in San Francisco in 1977 by Baker et al. [1] and our study. Both studies show a large number of prehospitalization deaths (51% compared to 66% in our study). Between arrival at the hospital and 7 days later, the percentages of deaths are similar; however, the percentage of late deaths ([7 days) in our study is only 2% compared to 12% in 1977. An explanation for a high incidence of prehospitalization deaths in our study is that the relative incidence of people dying from nonsurvivable injuries increases if the number of traumatic deaths per 100,000 is declining. The decrease in late deaths is likely to be caused by improved in-hospital trauma care (Fig. 4). Cothren et al. concluded that there had been a shift in the time to death; comparing the 1992 and 2002 data, there was a moderate shift from immediate to early deaths and a small shift from immediate to late deaths. Unfortunately, different time frames have been used in the two studies, so comparing the results is difficult [3, 9]. Another marked difference between the studies done during the 1970s and 1980s and recent studies is the mean age of the patients who suffer trauma-related deaths. Figure 5 shows the mean age of the deceased patients in the various studies. Note that during the last 30 years the mean age of the dead trauma patient has increased from the mid-30s to 43 years.

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The mean ISS in our study was 49. This is comparable to the study performed in San Diego in 1987 but is much higher than in the Denver study in 1992 (mean ISS 35). This can be explained by the fact that in our study only 14% of the deaths were caused by penetrating injury. In the Denver study 42% of the trauma deaths were related to penetrating injury, and in the San Diego study 30% (Fig. 6). Penetrating injury is undervalued in the ISS scoring system, so studies with many fatal penetrating injuries show a lower mean ISS [10]. When comparing the mechanisms of injury, our study shows that most of the deaths are caused by road and motor vehicle accidents (72%), whereas the U.S. studies are conducted in large U.S. cities and therefore have larger percentages of penetrating injuries causing death [1–3]. Cothren et al. concluded in their recent study that there is a decline in intentional injuries over the last decade. However, transport-related injuries in 10 years have increased: 43% transport-related injuries and 24% intentional injuries in 2002 compared to 34% transport-related and 40% intentional injuries back in 1992 [9]. In San Francisco in 1977, half the patients died of CNSrelated injuries. In our study one-third died of injuries to the CNS. The trend toward a decrease in CNS-related mortality has also been demonstrated by other authors [3]. Figure 7 shows the change in relative frequency of head injury- and hemorrhage-related deaths in the various studies. In San Francisco in 1977, the ratio of deaths related to brain injury/deaths related to bleeding was 1.61, whereas in Denver in 1992 this ratio was down to 1.27. In our study, as many people died due to CNS injury as those due to bleeding. Unfortunately, the recent Denver reassessment study has not included the causes of death because the data were acquired from death certificates and so contributing causes of death could not be identified [9]. An explanation for the change in the head injury/hemorrhage-related death ratio is the prevention of head injuries by the riders wearing protective helmets when on motorcycles and bicycles. In Baker et al.’s 1977 report, bleeding was the cause of death in almost one-third of the patients [1]. The same percentage was observed in the Denver study 15 years later [3]. Meislin et al. in 1997 also showed that a large percentage of patients (37%) died from hemorrhage [6]. Our study confirmed that after 30 years of trauma system development the same large percentage of patients (33%) still die from exsanguination. Despite all the improvements in trauma care, the percentage of exsanguination-related deaths has not declined over the last decades. A high percentage of bleeding is caused by aortic, chest, and pelvic fractures. To decrease the number of deaths from these injuries, a few strategies need to be outlined. First, prevention of aortic, chest, and pelvic injuries is the best was to avoid these fatal injuries. Multiple car safety

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precautions, such as improved car cage construction, seatbelts, and airbags have been made over the past decades to decrease the number and severity of injuries in motor vehicle accidents. Further improvements in safety devices are an ongoing process. Probably we cannot prevent accidents from happening, so we need adequate surgical input for early hemorrhage control in patients with major life-threatening bleeding injuries so they can reach the hospital adequately. The management of aortic and pelvic fractures associated with major bleeding is outlined in protocols in most major trauma centers these days. Angiography and embolization are increasingly used both as a diagnostic and therapeutic tool. Only 3% of the patients died of MOF compared with 7% and 10% in the other studies [1, 3] (Fig. 8). Many other recent studies have indicated a similar trend—that the incidence of lethal postinjury MOF is decreasing [3, 11, 12]. The development of MOF is multifactorial. Awareness of the syndrome has led to improved treatment of MOF. Lung-protecting ventilation, tight glucose control, adrenal replacement, and attenuation of its identified independent predictors have contributed to a decline in the incidence of MOF. In our study, death after 48 hours was uncommon. The decrease of late trauma deaths reflects a decrease in postinjury complications, which is likely due to improved trauma care in the hospital. The classic trimodal death distribution was recently challenged by New Zealand authors; they also described a distribution much more skewed toward the prehospital deaths [12].

Conclusions In all, 41% of trauma deaths are caused by LE trauma. Increasing age and co-morbidities have their reflection on the outcome after trauma. Because of the large number of elderly, compromised patients sustaining low falls, this group of patients has a large impact on the trauma management system. Strategies for preventing falls by elderly are a priority, and possibly specific protocols are needed for the management of trauma in the elderly [9, 13]. The injury mechanisms, time frames, and causes in Australia are different from those in the American experience. The classic trimodal death distribution in our study

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is much more skewed to early deaths, the patients are older, and the percentage of exsanguination is higher; moreover, MOF hardly exists. We report a low number of deaths per 100,000; however, the incidence of prehospitalization deaths in our study is higher than in other studies. As the number of traumatic deaths per 100,000 is declining, the relative incidence of people dying from nonsurvivable injuries during the prehospital phase will increase. Low-energy trauma is responsible for 41% of postinjury mortality with highly distinct epidemiology. This group deserves more attention and further investigation in the future.

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