Anatomic distribution and mortality of arterial injury in the wars in Afghanistan and Iraq with comparison to a civilian benchmark.

OBJECTIVE: The purpose of this study was to examine the anatomic distribution and associated mortality of combat-related vascular injuries comparing them to a contemporary civilian standard. DESIGN: The Joint Trauma Theater Registry (JTTR) was queried to identify patients with major compressible arterial injury (CAI) and noncompressible arterial injury (NCAI) sites, and their outcomes, among casualties in Iraq and Afghanistan from 2003 to 2006. The National Trauma Data Bank (NTDB) was then queried over the same time frame to identify civilian trauma patients with similar arterial injuries. Propensity score-based matching was used to create matched patient cohorts from both populations for analysis. RESULTS: Registry queries identified 380 patients from the JTTR and 7020 patients from the NTDB who met inclusion criteria. Propensity score matching for age, elevated Injury Severity Score (ISS; >15), and hypotension on arrival (systolic blood pressure [SBP] <90) resulted in 167 matched patients from each registry. The predominating mechanism of injury among matched JTTR patients was explosive events (73.1%), whereas penetrating injury was more common in the NTDB group (61.7%). In the matched cohorts, the incidence of NCAI did not differ (22.2% JTTR vs 26.6% NTDB; P = .372), but the NTDB patients had a higher incidence of CAI (73.7% vs 59.3%; P = .005). The JTTR cohort was also found to have a higher incidence of associated venous injury (57.5% vs 23.4%; P < .001). Overall, the matched JTTR cohort had a lower mortality than NTDB counterparts (4.2% vs 12.6%; P = .006), a finding that was also noted among patients with NCAI (10.8% vs 36.4%; P = .008). There was no difference in mortality between matched JTTR and NTDB patients with CAI overall (2.0% vs 4.1%; P = .465), or among those presenting with Glasgow Coma Scale (GCS) <8 (28.6% vs 40.0%; P = 1.00) or shock (SBP <90; 10.5% vs 7.7%; P = 1.00). The JTTR mortality rate among patients with CAI was, however, lower among patients with ISS >15 compared with civilian matched counterparts (10.7% vs 42.4%; P = .006). CONCLUSIONS: Mortality of injured service personnel who reach a medical treatment facility after major arterial injury compares favorably to a matched civilian standard. Acceptable mortality rates within the military cohort are related to key aspects of an organized Joint Trauma System, including prehospital tactical combat casualty care, rapid medical evacuation to forward surgical capability, and implementation of clinical practice guidelines. Aspects of this comprehensive combat casualty care strategy may translate and be of value to management of arterial injury in the civilian sector.

The life-saving effect of hyperbaric oxygenation during early-phase severe blunt chest injuries.

The effect of hyperbaric oxygenation (HBO2) on survival during the early phase of severe blunt chest injury (BChI) has not been elucidated. Our aim was to investigate this effect on human victims of BChI. We monitored cardiac index (CI), stroke volume index (SVI), PaO2 and PaO2/FiO2 in 18 victims treated conventionally, and 8 victims treated under combined conventional and HBO2 treatment. Out of the 18 victims, 4 survived (Group A) and 14 died (Group B). Another 8 victims, in Group C, received HBO, and all survived. Human victims showed marked reductions in all cardiorespiratory values during the first 24 h. Group B persistently tended towards a decrease in SVI, PaO2/FiO2 and PaO2, eventually reaching fatal levels. The survivors developed a cardiorespiratory function characterized by a tendency towards recovery of all monitored parameters, more notable in Group C, which showed an earlier and more significant normalization vs. Group A (P<0.01). Our clinical data suggest that the earliest possible HBO2 treatment after severe blunt trauma can significantly enhance victims' survival.

Traditional injury scoring underestimates the relative consequences of orthopedic injury.

OBJECTIVE: To demonstrate that patients with multiple injuries who have orthopedic injuries (ORTHO) face greater challenges regarding functional outcome than those without, to identify domains of postinjury dysfunction, and to illustrate the increasing discordance of functional recovery over time for ORTHO patients in relation to nonORTHO patients. METHODS: A convenience sample of adult blunt force trauma patients admitted to a Level I trauma center was evaluated at admission, and at 6 and 12 months after injury. Data were collected from the trauma registry (Trauma One), chart review, and interviews. Mailed surveys were completed 6 and 12 months after injury. The Short Form 36 (SF36) general health survey and the Sickness Impact Profile work scale (SIPw) were administered at both time points. Data are presented as mean +/- SEM or percent (%). To compare means, t tests were conducted, and Injury Severity Score (ISS) was controlled by linear regression before the evaluation of the role of ORTHO injury pattern on outcome measures. Significance is noted at the 95% confidence level (p < 0.05). RESULTS: The 165 patients studied averaged 37.2 +/- 1.1 years in age and were 67% men. The mean ISS was 14.4 +/- 0.6 and 61% had ORTHO injury. ORTHO patients were no different from nonORTHO in any measure of baseline status including the SIPw score and all domains of the SF36, except that the ISS was greater in the ORTHO group (15.6 +/- 0.96 vs. 12.7 +/- 0.73, p = 0.017). Baseline SF36 values were similar to national norms. Follow-up was 75% at 6 months, and 51% at 12 months. Those lost to follow-up differed only in that they were more likely to be men. Sixty-four percent had returned to work 12 months after injury. After controlling for ISS with linear regression, the ORTHO patients had worse scores on all physical measures of the SF36 (bodily pain, physical function, and role-physical). By 12 months after injury, the relative dysfunction of the ORTHO patients had expanded to include the SIPw score (p = 0.016) and six of eight SF36 domains (bodily pain, physical function, role-physical, mental health, role-emotional, and social function, all p < 0.05). CONCLUSION: Injury severity affects both mortality and the potentially more consequential issues of long-term morbidity. Patients with ORTHO injury have relatively worse functional recovery, and this worsens with time. As trauma centers approach the limits of achievable survival, new advances in trauma care can be directed more toward the quality of recovery for our patients. This will be contingent on further development of screening, scoring, and treatment systems designed to address issues of functional outcome across injury boundaries for those who survive.

Endogenous adenosine and secondary injury after chest trauma.

BACKGROUND: No previous studies have examined actions of adenosine or related compounds after blunt chest trauma, but we have shown that the prototype adenosine-regulating agent, acadesine (aminoimidazole carboxamide ribonucleotide [AICAR]), has multiple favorable anti-inflammatory actions after other forms of trauma, ischemia, hemorrhage, and sepsis; and that a progressive inflammatory response in the contralateral (uninjured) lung after unilateral blunt chest trauma is caused (in part) by activation and sequestration of circulating leukocytes (white blood cells [WBCs]). Thus, we hypothesized that AICAR would ameliorate WBC-dependent, secondary pathophysiologic changes after blunt chest trauma. METHODS: Mongrel pigs (28+/-1 kg, n = 21) were anesthetized, mechanically ventilated, and injured on the right chest (pulmonary contusion) with a captive bolt gun. Either AICAR (1 mg/kg + 0.2 mg/kg/min) or its saline vehicle were administered for a 12-hour period, beginning 15 minutes before injury. RESULTS: Injury caused a three- to fourfold increase in bronchoalveolar lavage (BAL) WBC counts, 10- to 20-fold increases in BAL protein, and 200% increases in lung edema as measured by wet-dry ratio (all p < 0.05), in both the injured (right) and the noninjured (left) lungs. With AICAR versus saline, BAL WBC counts, lung myeloperoxidase levels, and systemic hemodynamics were similar. However, the increases in BAL protein were attenuated by 30% to 50% (p < 0.14, NS) and edema was reduced (p < 0.05) in both lungs. Furthermore, oxygenation, hypercapnia, acidosis (all p < 0.05), and survival were improved (9 of 10 vs. 4 of 11, p < 0.04). CONCLUSION: Pretreatment with AICAR before experimental pulmonary contusion ameliorates the trauma-induced destruction of the alveolar capillary membrane, and attenuates the delayed secondary injury in the contralateral uninjured lung, by a mechanism that may be independent of leukocytes. Endogenous adenosine could have a role in the pathophysiologic response after blunt chest injury, with potential sites of action including the endothelium and alveolar macrophage. Adenosine-regulating agents may have therapeutic potential after blunt chest injury, but further studies are needed in clinically relevant models, with administration begun at the time of resuscitation.

Predicting inpatient mortality for pediatric trauma patients with blunt injuries: a better alternative.

PURPOSE: The aim of this study was to identify significant independent predictors of inpatient mortality rates for pediatric victims of blunt trauma and to develop a formula for predicting the probability of inpatient mortality for these patients. METHODS: Emergency department and inpatient data from 2,923 pediatric victims of blunt injury in the New York State Trauma Registry in 1994 and 1995 were used to explore the relationship between patient risk factors and mortality rate. A stepwise logistic regression model with P<.05 was developed using survival status asthe dependent variable. Independent variables included are elements of the Pediatric Trauma Score (PTS), additional elements from the Revised Trauma Score (RTS), the motor response and eye opening components of the Glasgow Coma Scale (GCS), age-specific systolic blood pressure, the AVPU score, and 2 measures of anatomic injury severity (the Injury Severity Score [ISS] and the International Classification of Disease, Ninth Revision-based Injury Severity Score [ICISS]). RESULTS: The only significant independent predictors of severity that emerged were the ICISS, no motor response (best motor response = 1) from the GCS, and the unresponsive component from the AVPU score. The statistical model exhibited an excellent fit (C statistic = .964). The specificity associated with the prediction of inpatient mortality rate based on the presence of 1 or more of these risk factors was .926, and the sensitivity was .944. CONCLUSION: The best independent predictors of inpatient mortality rate for pediatric trauma patients with blunt injuries include variables not specifically contained in the PTS or the RTS: ICISS, no motor response (best motor response = 1) from the GCS, and the unresponsive component of the AVPU score.

Effect of hypoxia or hyperbaric oxygen on cerebral edema following moderate fluid percussion or cortical impact injury in rats.

This study was designed to evaluate the production of cerebral edema [as measured by tissue specific gravity (SpG)] following moderate fluid percussion (FP) and cortical impact (CI) injury in rodents. To determine the effects of a secondary systemic insult, hypoxia (13% oxygen for 30 min) was added to some experimental groups immediately after head injury. To determine the effects of hyperbaric oxygen (HBO) on injured cortical tissue, additional animal groups were exposed to HBO (1.5 atm, for 60 min), beginning 4 h after head trauma. Both injury models produced equal amounts of tissue edema at the site of injury (mean SpG +/- SEM = 1.035 +/- 0.001), when measured 6 h posttrauma. There was no significant edema at the tissue sites immediately adjacent to the trauma sites. The addition of hypoxia to either injury system did not increase edema formation beyond that produced by injury alone. HBO reduced the water content of the trauma site in animals that had received FP, but not in animals receiving CI. We conclude that with the injury parameters used in this protocol, both FP and CI appear to produce focal cerebral edema at the site of trauma. Hypoxia does not worsen edema. HBO appears to reduce edema produced by FP, but not by CI.

Blunt diaphragm injuries. A five-year experience.

Between 1983 and 1988, 33 (21 men, 12 women) patients were treated for blunt diaphragmatic injuries following motor-vehicle (90%) or auto-pedestrian (10%) accidents at the Presley Trauma Center. Thirteen patients (39%) were right sided and 19 (56%) were left sided. One patient sustained bilateral ruptures. The mean Injury Severity Score (ISS) in both those that lived and those that died was not significantly different when right- and left-sided injuries were compared. Admission chest films were abnormal in 28 patients and diagnostic in nine patients (27%). The chest x ray was abnormal in 10 (78%) of those with right-sided injury. Twenty-three patients had diagnostic peritoneal lavage (DPL); 19 were initially positive, two were initially negative but became positive on relavage. There were two false-negative lavages. CT scan (4 patients) and barium enema (1 patient) were nondiagnostic. Diagnosis was delayed in four patients, two were diagnosed by repeat chest x ray and two by repeat lavage. All patients had multiple associated injuries, with 82 per cent having concomitant intra-abdominal injuries. All patients were explored via the transabdominal route. Complications occurred in 55 per cent and there were eight deaths (24%), all unrelated to the diaphragmatic injury. There was no relationship to mortality and hemidiaphragm injured. Chest x ray remains the single most beneficial diagnostic test for diaphragmatic injury. DPL is an insensitive test for isolated diaphragm injuries; however, the combination of CXR and DPL will lead to the diagnosis in the majority of cases. Ancillary radiologic tests are not beneficial. An elevated or obscured right hemidiaphragm should raise suspicion for blunt rupture.(ABSTRACT TRUNCATED AT 250 WORDS)