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A rapid computed tomography technique or "trauma scan" (TS) provides high-resolution studies of the head, cervical spine, chest, abdomen, and pelvis. We sought to determine whether TS has decreased missed injuries. A previous study of TS found a 3% missed rate.After institutional review board approval, trauma patients from January 2001 through December 2008 were reviewed for delayed diagnosis (DD) of injury to the head, cervical spine, chest, abdomen, or pelvis. Missed extremity injuries were excluded. Injury Severity Score, length of stay, type of injury, outcomes, and days to detection were captured.Of 26,264 patients reviewed, 90 patients had DD, with an incidence of 0.34%. DD most commonly presented on day 2. Injuries included 16 bowel/mesentery, 12 spine, 11 pelvic, 8 spleen, 6 diaphragm, 5 clavicle, 4 scapula, 4 cervical spine, 4 intracranial, 4 sternum, 3 maxillofacial, 3 liver, 2 heart/aorta, 2 vascular, 2 urethra/bladder, 2 pneumothorax, and 2 pancreas/common bile duct. DD resulted in 1 death, 6 prolonged intensive care unit stays, 19 operative interventions, and 38 additional interventions.TS is an effective way of evaluating trauma patients for intracranial, cervical spine, chest, abdomen, and pelvic injuries that have the potential to impact morbidity and mortality. The incidence of injuries missed in these crucial areas has been reduced at our institution by the use of this radiographic modality. The most common missed injury remains bowel, and so a high index of suspicion and the tertiary survey must remain a mainstay of therapy.

Burn injury is associated with a decline in glucose utilization and insulin sensitivity due to alterations in postreceptor insulin signaling pathways. We have reported that blockade of the renin-angiotensin system with losartan, an angiotensin II type 1 (AT1) receptor blocker, improves whole body insulin sensitivity and glucose metabolism after burn injury. This study examines whether losartan improves insulin signaling pathways and insulin-stimulated glucose transport in skeletal muscle in burn-injured rats. Rats were injured by a 30% full-skin-thickness scalding burn and treated with losartan or placebo for 3 days after burn. Insulin signaling pathways were investigated in rectus abdominus muscle taken before and 90 s after intraportal insulin injection (10 U·kg−1). Insulin-stimulated insulin receptor substrate 1-associated phosphatidylinositol 3-kinase and plasma membrane-associated GLUT4 transporter were substantially increased with losartan treatment in burn-injured animals (59% above sham). Serine phosphorylated AKT/PKB was decreased with burn injury, and this decrease was attenuated with losartan treatment. In a separate group of rats, the effect of insulin on 2-deoxyglucose transport was significantly impaired in burned as compared with sham soleus muscles, in vitro; however, treatment of burned rats with losartan completely abolished the reduction of insulin-stimulated 2-deoxyglucose transport. These findings demonstrate a cross talk between the AT1 and insulin receptor that negatively modulates insulin receptor signaling and suggest a potential role of renin-angiotensin system blockade as a therapeutic strategy for enhancing insulin sensitivity in skeletal muscle and improving whole-body glucose homeostasis in burn injury.

Trauma during pregnancy places two lives at risk. Knowledge of risk factors for trauma during pregnancy may improve outcomes.We reviewed the charts of 188 such patients admitted to a Level I trauma center from 1996 to 2004. A comparison was made of injury severity and outcome from a cohort of nonpregnant female trauma patients selected with a similar temporal occurrence and age range.Motor vehicle collisions comprised 160 cases, 67 using a restraint device. Of 84 patients tested, 45 tested positive for intoxicants, 16 positive for 2 or more intoxicants. A significant trend toward less testing through the study period was observed (p = 0.0002). Injury severity was assessed by Revised Trauma Score (RTS). RTS11 or admission to operating room or intensive care units (OR/ICU) classified patients as severely injured. The six maternal fatalities had an RTS11 or OR/ICU disposition. Fetal outcomes included 155 live in utero, 18 live births, and 15 fatalities correlating with injury severity by either criteria (p0.0001). Of the fetal fatalities, 7 occurred with RTS = 12, but only 3 fatalities occurred in the 147 cases not admitted to OR/ICU. Gestational age correlated (p0.0001) with fetal outcomes. The 18 live births had mean gestational ages of 35 +/- 4 weeks as compared with fetal fatalities at 20 +/- 9 weeks, and fetuses alive in utero at 22 +/- 9 weeks gestation. Coagulation tests prothrombin time (PT), international normalized ratio (INR) (both p0.008), and partial thromboplastin time (PTT) (p0.0001) correlated with maternal outcome. A matched cohort of nonpregnancy trauma cases during the same time frame indicated that, despite a significantly higher percentage of severely injured patients, fewer fatalities occurred. This might reflect a greater risk for the pregnant trauma patient.This study of trauma in pregnancy cases revealed a high percentage with risk behaviors. There was a significant trend toward less intoxicant testing in recent years. Coagulation tests were the most predictive of outcomes. Lower gestational age correlated with fetal demise.

Insulin resistance after burn is associated with alterations in postreceptor insulin signaling and abnormal glucose homeostasis. The renin-angiotensin system (RAS) exerts a largely inhibitory role on insulin action and is activated after burn injury. We hypothesized that upregulation of RAS is involved in the development of insulin resistance in burned rats. We examined the possibility that an angiotensin II type 1 (AT1) receptor blocker, losartan, enhances insulin sensitivity and thereby increases glucose tolerance in thermally injured rats. A 30% body surface area burn was induced by immersion of the dorsum into water with a temperature level of 95 degrees C for 15 s. Sham-burned rats were immersed in water with a temperature level of 23 degrees C. Losartan (30 mg/kg per day) or placebo (water) was given by gavage immediately after the burn injury and daily for 3 days postburn injury, resulting in sham-burned, burn placebo, and burn losartan groups. Plasma angiotensin II levels between burn placebo and sham-burned groups were not different 3 days after burn injury. However, losartan significantly increased plasma angiotensin II levels (P0.05), suggesting blockade of the AT1 receptor. An oral glucose tolerance test was performed 3 days postburn injury. There was an increase in the area under the curve for insulin and the glucose insulin index in burn placebo group as compared with sham-burned group, indicating insulin resistance. Losartan treatment abolished the insulin resistance in burn as evidenced by an area under the curve for insulin and glucose insulin index lower than that in the burn placebo group and similar to that in the sham-burned group. This suggests that insulin resistance and glucose intolerance associated with burn injury is, in part, caused by RAS.

Although it may be apocryphal, it is said that the Chinese have a curse that states, “May you live in interesting times.” We live in interesting times. Hospitals across the country are facing financial difficulty and trauma centers are the first area examined for closure. Trauma centers in Pennsylvania, West Virginia, and Las Vegas have closed, at least temporarily, because of problems with specialist coverage. The insurance crisis in many of our states has created a situation where even physicians who are willing to care for trauma patients cannot get professional liability coverage, forcing them to either move to more physician friendly states, to come up with new alternatives such as physician or specialty owned carriers, or even to go bare. A flaw in the Medicare reimbursement formula has lead to a 10% decrease in physician payments over two years. And, even though Medicare does not pay a large role in trauma reimbursement, we all know that as Medicare does, other carriers rapidly follow. Leapfrog and other consumer groups are demanding “quality care” and are determining what that quality is, whether we agree with it or not. This quest for quality has lead to the 80 hour workweek for residents, which leads us to wonder how we will do the work we need to do and says nothing of how we will educate residents with these limitations. Finally, despite these restrictions, we still face the issue that medical students are not choosing surgical residencies as they did before, and surgical residents are not choosing trauma fellowships for training. How can trauma surgery and trauma surgeons survive in the current economic environment of medicine? Surely there have never been such interesting (and dangerous) times for our field? As most presidents do in preparing their presidential addresses, I went back and reviewed the addresses of my predecessors to gain historical perspective and to reexamine their wisdom. In doing that, I learned once again that there are no new problems in medicine—whatever problems appear new at the time have almost certainly been considered in the past, even if the tools were not available to address them. This also applies to the problems I am considering today. Our first president, Kimball Maull, talked about the disconnect between the public perception of trauma and the actual problem that trauma presents to society. Our second president, Burton Harris, talked about the problems of the redefinition of surgery and the surgical specialties, the lack of interest of many surgeons in doing trauma, and most fearsome of all, the evil effects of business on the field of medicine. Len Jacobs talked about the forces of diversification and specialization which were affecting trauma care and noted that “Uncompensated trauma care and maldistribution of trauma centers Submitted for publication May 7, 2003. Accepted for publication May 12, 2003. Copyright © 2003 by Lippincott Williams & Wilkins, Inc. From the Division of Trauma/Critical Care, University of Tennessee Medical Center, Knoxville, Tennessee. Presidential address presented at the 16th Annual Scientific Assembly of the Eastern Association for the Surgery of Trauma, January 15–18, 2003, Ft. Myers, Florida. Address for correspondence: Blaine L. Enderson, MD, MBA, FACS, FCCM, Professor of Surgery and Chief, Division of Trauma/Critical Care, University of Tennessee Medical Center at Knoxville, Department of Surgery, University Memorial Hospital, 1924 Alcoa Highway, Knoxville, Tennessee, 37920-6999; email: benderso@utk.edu.

Purpose: The surgical resident experience with trauma has changed. Many residents are exposed to predominantly nonoperative patient care experiences while on trauma rotations. Data from a large multicenter study were analyzed to estimate surgical resident exposure to trauma laparotomy, diagnostic peritoneal lavage (DPL), and focused abdominal sonography for trauma (U/S). Methods: Centers completed a self-report questionnaire on their institutional demographics, admissions, and procedure for a 2-year period (1998-1999). Results: A total of 82 trauma centers that provide resident teaching were included. The included centers represent over 247,000 trauma admissions. The majority of trauma centers (65.9%) had > 80% blunt injury. Although all centers performed laparotomies, other results were more variable. For U/S, 24.2% performed none at all and 47.0% performed fewer than two U/S examinations per month. For DPLs, 3.8% performed none and 66.7% performed fewer than two per month. Assuming 1 night of 4 on call, the average surgical resident training at a trauma center performing > 80% blunt trauma has the potential to participate in only 15 trauma laparotomies, 6 diagnostic peritoneal lavages, and 45 ultrasound examinations per year. In addition, the resident will care for an average of 500 blunt trauma patients before performing a splenectomy or liver repair. Conclusion: Surgical resident experience on most trauma services is heavily weighted to nonoperative management, with a relatively low number of procedures, little experience with DPL, and highly variable experience with ultrasound. These data have serious implications for resident training and recruitment into the specialty.

Background: Proinflammatory eicosanoids formed from arachidonic acid (AA) by lipoxygenase (LO) and cyclooxygenase (COX) pathways have been shown to inhibit apoptosis in certain cell types. This study determined whether inhibition of LO and COX increased apoptosis in AA-treated HL-60 cells in vitro. Methods: HL-60 cells were incubated with 50 μmol/L AA and an enzyme inhibitor (1-10 μmol/L) for COX, LO, 12-LO, and 5-LO for 12 hours. Flow cytometry was used to assess viability, apoptosis, and necrosis. Apoptosis was further assessed using terminal dUTP nick end-labeling and DNA fragmentation. Results: The highest concentration of LO inhibitors, but not COX inhibitors, decreased viability and increased apoptosis and necrosis in the presence of exogenous AA. Conclusion: These results suggest that disruption of the metabolism of AA by LO, in particular 5-LO, decreases cell survival and increases apoptosis. Thus, downstream metabolic processing of AA by LO but not COX plays a critical role in the regulation of HL-60 cell apoptosis.

Background: The differentiation of duodenal perforation from duodenal hematoma is not always possible with computed tomography (CT). Our diagnostic guideline has included duodenography to investigate CT findings of periduodenal fluid or wall thickening. However, the utility of duodenography as a diagnostic study in blunt abdominal trauma is not defined. We evaluated duodenography as a diagnostic test in patients with suspected blunt duodenal injuries (BDIs). Methods: During a 10-year period, 96 patients out of 25,608 trauma admissions had CT findings of possible BDI and underwent duodenography. Demographic and clinical data, diagnostic methods, and management were derived from prospectively collected data. CT and duodenography studies were reviewed and correlated with surgical findings and outcome. All CT scans were obtained with intravenous contrast; oral contrast was used in 32 patients. Duodenography was analyzed using the 2 x 2 method and Bayes theorem. Results: Indications for duodenography included periduodenal fluid without extravasation (76%), abnormal duodenal wall thickening (16%), and retroperitoneal extraluminal gas (5%). Eighty-six duodenography studies were reported as normal, six were consistent with hematoma, one was indeterminate, and only three revealed extravasation. Two of these three patients with duodenal perforation had retroperitoneal extraluminal air. Only one patient underwent exploration on the basis of duodenography. No blunt duodenal perforation was diagnosed by CT. Overall, duodenography had sensitivity of 54% and specificity of 98%. For BDIs requiring repair, duodenography sensitivity was only 25%; the false-negative rate was also 25%. Retroperitoneal extraluminal air was a useful sign of duodenal perforation, occurring in two of three patients with BDI and only in one without BDI (p < 0.001). Conclusion: Duodenography has a low sensitivity in patients with suspected BDI by CT findings and is of minimal utility in diagnostic evaluation. Retroperitoneal extraluminal air seen on CT is an important sign of BDI requiring surgical repair.

We measured D-dimer and plasminogen activator inhibitor-1 (PAI-1) activity in 45 trauma patients to assess their efficacy in predicting the post-traumatic hemostatic perturbations. We found the correlation between D-dimer measured by Simpli Red test and ELISA to be highly significant (p=0.0001). The D-dimer ELISA indicated that the serial changes of D-dimer after trauma were variable. However, the increases of D-dimer were associated with clinical conditions of the patient, such as trauma surgery, infections, or thrombotic complications. A significant correlation was found for D-dimer levels measured by ELISA versus the injury severity score (ISS) in all the trauma patients on day 1 (p=0.0153) and on day 2 (p=0.0495). The PAI-1 activity was increased at admission and showed a progessive decline from day 2 onward, and the correlation for the daily decline of PAI-1 was highly significant (p=0.0001). The PAI-1 activity and plasminogen activator activity showed a significant negative correlation on days 1, 2, and 3. PAI-1 activity correlated moderately with D-dimer level only on day 1 (p=0.0569). Three out of forty-five patients developed thrombotic complications: one patient who died from pulmonary embolism and two patients who developed adult respiratory distress syndrome (ARDS). In summary: 1) PAI-1 activity and D-dimer exhibited contrasting serial changes after trauma. 2) There was also a negative correlation between PAI-1 activity and PA activity. 3) A significant correlation of D-dimer with ISS confirms, as might be anticipated, that there is increased activation of the coagulation mechanism in severe injury, and suggests that D-dimer levels may prove useful to screen for patients at strong risks of thrombotic complications.

Occult pneumothorax is defined as a pneumothorax that is detected by abdominal computed tomographic (CT) scanning, but not routine supine screening chest roentgenograms. Forty trauma patients with occult pneumothorax were prospectively randomized to management with tube thoracostomy (n = 19) or observation (n = 21) without regard to the possible need for positive pressure ventilation, to test the hypothesis that tube thoracostomy is unnecessary in this entity. Eight of the 21 patients observed had progression of their pneumothoraces on positive pressure ventilation, with three developing tension pneumothorax. None of the patients with tube thoracostomy suffered major complications as a result of the procedure. Hospital and ICU lengths of stay were not increased by tube thoracostomy. Patients with occult pneumothorax who require positive pressure ventilation should undergo tube thoracostomy.

This study examined a mesh wrap technique that provides effective hepatic tamponade and clinical experience with the technique in 6 patients is reported. Technical feasibility and effectiveness were investigated in 8 miniature swine. The animals were divided into two groups: group A (n = 4), control animals; stellate liver lacerations without mesh wrap or other measures for hemostasis, and group B (n = 4); stellate liver laceration with synthetic absorbable mesh wrap applied for hepatic hemostasis. Except for mesh application, all variables were held constant for both groups. All animals in the control group died within 20 to 120 minutes (mean: 65 minutes). All animals in group B survived (p = 0.029). The livers were harvested for gross and microscopic examinations. No abscess, bile leak, or hematoma was noted. Clinically, total mesh wrapping was attempted in 6 patients with blunt exsanguinating liver injuries. The technique failed intraoperatively in two patients with juxtacaval lacerations and hepatic vein avulsion injuries. One patient with a bilobar gunshot wound died later of sepsis. In three patients with bursting injuries, the technique successfully controlled bleeding and resulted in long-term survival. In conclusion, the total hepatic mesh wrap (1) is geometrically, technically, and mechanically feasible, (2) was not associated with complications in this series, and (3) can effectively secure hemostasis following parenchymal liver injury.