Western Trauma Association

: Motor vehicle crashes are the leading cause of death among teenagers because of higher crash rates per mile driven and low seat belt use rates. : An educational program aimed at increasing seat belt use among teens was implemented at five area high schools in the spring of 2007 and six high schools in the fall of 2007. Observational studies were conducted as students arrived at school. Resources and incentives were provided to generate peer-to-peer motivation. Schools competed against one another to see which could achieve the highest seat belt usage rate during a 7-week period. Observational studies were repeated, and success of the safety campaign was measured by an increase in seat belt usage at the participating high schools. : At the beginning of the safety campaign, average seat belt use among teen drivers was 47% and 59% for the spring and fall, respectively. Teen passengers had an average usage of 40% and 57% for the spring and fall. In the spring campaign, seat belt use increased by 36% and 19% for teen drivers and passengers, respectively. Similar results were seen in the fall, with increases of 26% and 13% for teen drivers and passengers, respectively. Overall seat belt use in both campaigns increased by 20%, to an average use rate of 71%. : Social pressure and poor comprehension of the risks of injury were identified as barriers to seat belt usage among teenage high school students. A friendly, competitive approach to openly discussing and educating teens about these risks led to a 20% increase in seat belt usage among teen drivers and their passengers.

As the number of US burn centers has declined, access to burn care is increasingly limited. Inexperience in burn wound assessment by referring physicians often results in overtriage or undertriage. In an effort to improve access to burn care in our region, we instituted a program of telemedicine evaluation of acute burns. We created a telemedicine network linking our burn center to three hospitals located 298 to 350 air miles away. Participants agreed to perform telemedicine consultation for acutely burned patients admitted to their emergency departments. We compared consults and referrals from these facilities during the period July 2005 to August 2007 (TELE) to those during a 2-year period before instituting telemedicine (PRE-TELE). During the TELE period, 80 patients were referred, of whom 70 were seen acutely by telemedicine, compared with 28 PRE-TELE referrals. The groups did not differ in age or burn size. Only 31 patients seen by telemedicine received emergency air transport (44.3%), compared with 100% of PRE-TELE patients (p < 0.05). Nine other TELE patients were transported by family; 30 other patients were treated locally. Ten remaining patients were transported without telemedicine evaluation. TELE patients transported by air had somewhat larger burn sizes (9.0% vs. 6.5% total body surface area; p = NS) and longer length of stay (13.0 days vs. 8.0 days; p = NS) than PRE-TELE patients. Burn size estimates by burn center physicians made either by telemedicine or direct inspection correlated closely but both differed significantly from those of referring physicians. Providers and patients expressed a high level of satisfaction with the telemedicine experience. Acute evaluation of burn patients can be performed accurately by telemedicine. This can reduce undertriage or overtriage for air transport, improve resource utilization, and both enhance and extend burn center expertise to many rural communities at low cost.

Gastric function in trauma patients is poorly understood. In animals, shock causes gastric luminal alkalinization and bile reflux. In trauma patients, studies of stress gastritis prophylaxis demonstrated with continuous gastric pH monitoring that the stomach became alkaline even without antisecretory therapy. Therefore, we hypothesized that trauma patients have an alkaline gastric environment that may be because of bile reflux. A prospective observational study at an urban Level I trauma center was performed. All major torso trauma patients (severe head injuries excluded) who met the criteria for standardized shock resuscitation were eligible for inclusion. A 12.5 Fr silastic pH probe (Sandhill Scientific) was placed in the stomach and the gastric pH continuously monitored for 7 days. Patients received no stress gastritis prophylaxis. Gastric samples were obtained each day and assayed for total bile acids and pH. Twelve patients were entered into the study. Mean age was 31 years +/- 4 years, 67% men, 75% blunt mechanism of injury, and mean Injury Severity Score 28 +/- 3. Three patients (25%) developed multiple organ failure and four acquired ventilator-associated pneumonia. During the first day of continuous pH monitoring, 9 of 12 patients had a gastric pH >4 for the majority of the day with 7 patients having essentially no acid production. During subsequent days, gastric pH began to drop and by the 4th day the majority of each day was spent at a pH <4. Additionally, gastric pH of patients with ventilator-associated pneumonia or multiple organ failure tended to be more alkaline. Bile acid was present in the gastric fluid of all patients in varying amounts. However, there was no significant correlation between gastric pH and bile acid concentration. Traumatic injury causes gastric luminal alkalinization that may be related, only in part, to bile acid reflux. Other alkalinizing factors remain to be elucidated.

Previously, we had shown that elevation of cerebral perfusion pressure, using pressors, improved short-term outcomes after traumatic brain injury and hemorrhagic shock in swine. The current study evaluates outcomes after resuscitation with diaspirin cross-linked hemoglobin (DCLHb)--a hemoglobin-based oxygen carrier with pressor activity--in the same swine model of traumatic brain injury and hemorrhagic shock. Anesthetized and ventilated swine received traumatic brain injury via cortical fluid percussion (6-8 atm) followed by 45% blood volume hemorrhage. One hour later, animals were randomized to either a control group (SAL) resuscitated with normal saline equal to three times shed blood volume or to one of two experimental groups resuscitated with DCLHb. The two experimental groups consisted of a low-dose group, resuscitated with 250 mL of DCLHb (Hb1), and a high-dose group, resuscitated with 500 mL of DCLHb (Hb2). Animals were observed for 210 minutes postresuscitation. Outcomes evaluated were cerebral oxygenation by measuring partial pressure and saturation of oxygen in cerebrovenous blood; cerebral function by evaluating the preservation and magnitude of cerebrovascular carbon dioxide reactivity; and brain structural damage by semiquantitatively assessing beta amyloid precursor protein positive axons. Postresuscitation, cerebral perfusion pressure was higher in the DCLHb groups (p < 0.05, Hb1 and Hb2 vs. SAL), and intracranial pressure was lower in the Hb2 group (p < 0.05 vs. SAL). Cerebrovenous oxygen level was similar in all groups (p > 0.05). At baseline, 5% carbon dioxide evoked a 16 +/- 1% increase in cerebrovenous oxygen saturation, indicating vasodilatation. At 210 minutes, this response was nearly absent in SAL (4 +/- 4%) (p < 0.05 vs. baseline) and Hb1 (1 +/- 5%), but was partially preserved in Hb2 (9 +/- 5%). There was no intergroup difference in beta amyloid precursor protein positive axons. Five of 20 SAL and 0 of 13 DCLHb animals developed brain death (flat electroencephalogram) (p = 0.05, SAL vs. DCLHb). Postresuscitation, DCLHb animals maintained higher mean pulmonary arterial pressure (28 +/- 1 mm Hg, SAL; 42 +/- 1 mm Hg, Hb1; 45 +/- 1 mm Hg, Hb2) (p < 0.05, Hb1 and Hb2 vs. SAL) and lower cardiac output (3.9 +/- 1.6 L/min, SAL; 2.6 +/- 0.1 L/min, Hb1; 2.7 +/- 0.1 L/min, Hb2) (p < 0.05, Hb1 and Hb2 vs. SAL). Three Hb2 animals died as a result of cardiac failure, and one SAL animal died as a result of irreversible shock. In this swine model of traumatic brain injury and hemorrhagic shock, resuscitation with DCLHb maintained a higher cerebral perfusion pressure. Low-dose DCLHb (minimal increase in oxygen carriage) failed to significantly improve short-term outcome. With high-dose DCLHb (significant improvement in oxygen carriage), intracranial pressure was lower and cerebrovascular carbon dioxide reactivity was partially preserved; however, this was at the cost of poorer cardiac performance secondary to high afterload.

To provide preliminary data on the resolution profile of aortic intimal injuries treated nonoperatively and on the safety of nonoperative management of these injuries. Five blunt trauma patients diagnosed by transesophageal echocardiography (TEE) with traumatic intimal injury of the aorta were assigned to nonoperative management. This included beta-blockade to maintain systolic blood pressure between 80 and 90 mm Hg and heart rate between 60 and 80 beats/min, serial TEE studies, and invasive monitoring in the intensive care unit. The evolution of injury, the effectiveness of nonoperative treatment, and the potential need for an operative intervention were monitored. The patients had a mean Injury Severity Score of 32 and sustained multiple associated thoracic and extrathoracic injuries. Aortic injuries were located at the level of the ligamentum arteriosum and in the descending aorta adjacent to the diaphragm in three and two patients, respectively. The mean size of injury was 12.5 mm (range, 5-20 mm) and a thrombus attached to the endothelium was present in three of the five patients. Complete resolution of injury occurred within 9.4 +/- 6.6 days (range, 3-19 days). All patients remained hemodynamically stable and adequately perfused. All demonstrated progressive resolution of their aortic intimal injuries. No complications related to the aortic injuries were identified during a mean follow-up of 16.8 months. This small series suggests that aortic intimal injuries smaller than 20 mm in hemodynamically stable patients treated with beta-blockade resolve within several days. This approach appears safe when monitored by serial TEE studies performed by experienced experts, and continuous invasive hemodynamic monitoring.

Patients with major fracture/soft-tissue injuries are at risk for adult respiratory distress syndrome after secondary infection. Fracture fluids (FF) are rich in neutrophil (PMN) -specific chemokines such as interleukin-8. PMN respond to both interleukin-8 and bacterial stimuli with calcium ([Ca2+]i) fluxes, which can initiate respiratory burst (RB). We hypothesize that small amounts of FF entering the circulation could exaggerate PMN [Ca2+]i and RB responses, potentially increasing the risk of adult respiratory distress syndrome. FF were obtained from 10 patients at open fixation of the femur 2 to 5 days postinjury. Volunteer PMN were isolated and loaded with fura dye. PMN were preincubated either in 30% autologous plasma (AP)/70% buffer, or in 5% FF/25% AP/70% buffer. Cells were resuspended in buffer with 1,2,3-dihydrorhodamine and stimulated with low-dose n-formyl-methionyl-leucyl-phenylalanine (fMLP). [Ca2+]i was assayed by fura fluorescence at 505 nm after excitation at 340/380 nm. RB was assessed by 1,2,3-dihydrorhodamine fluorescence at 530 nm after 488 nm excitation. PMN basal [Ca2+]i was higher after FF incubation than AP incubation (94+/-12 vs. 61+/-9 nmol/L, p = 0.0002). Peak [Ca2+]i response to fMLP was 475+/-47 nmol/L after FF but only 356+/-22 nmol/L after AP (p = 0.01). Two hundred seconds after fMLP, [Ca2+]i remained higher after FF (172+/-17 vs. 145+/-9 nmol/L, p = 0.04). Basal RB was slightly higher after FF than AP (13.4+/-0.3 vs. 11.3+/-0.3 units, p = 0.051) as was the maximal rate of extracellular oxidant release (1.10+/-0.17 vs. 0.76+/-0.16 units/s, p = 0.004) and total oxidant production (42.5+/-0.8 vs. 31.7+/-0.8 units, p = 0.006). Small amounts of FF in plasma can exaggerate PMN [Ca2+]i flux and RB responses to subsequent bacterial stimuli. These findings are consistent with the hypothesis that release of FF into the circulation primes PMN and, thus, may predispose to adult respiratory distress syndrome. Such PMN priming events might have important implications for both the operative and medical management of patients with major fractures.