Pathophysiology in patients with polytrauma.

The pathophysiology after polytrauma represents a complex network of interactions. While it was thought for a long time that the direct and indirect effects of hypoperfusion are most relevant due to the endothelial permeability changes, it was discovered that the innate immune response to trauma is equally important in modifying the organ response. Recent multi center studies provided a "genetic storm" theory, according to which certain neutrophil changes are activated at the time of injury. However, a second hit phenomenon can be induced by activation of certain molecules by direct organ injury, or pathogens (damage associated molecular patterns, DAMPS - pathogen associated molecular patterns, PAMPS). The interactions between the four pathogenetic cycles (of shock, coagulopathy, temperature loss and soft tissue injuries) and cross-talk between coagulation and inflammation have also been identified as important modifiers of the clinical status. In a similar fashion, overzealous surgeries and their associated soft tissue injury and blood loss can induce secondary worsening of the patient condition. Therefore, staged surgeries in certain indications represent an important alternative, to allow for performing a "safe definitive surgery" strategy for major fractures. The current review summarizes all these situations in a detailed fashion.

Viscoelastic measurements of platelet function, not fibrinogen function, predicts sensitivity to tissue-type plasminogen activator in trauma patients.

BACKGROUND: Systemic hyperfibrinolysis is a lethal phenotype of trauma-induced coagulopathy. Its pathogenesis is poorly understood. Recent studies have support a central role of platelets in hemostasis and in fibrinolysis regulation, implying that platelet impairment is integral to the development of postinjury systemic hyperfibrinolysis. OBJECTIVE: The objective of this study was to identify if platelet function is associated with blood clot sensitivity to fibrinolysis. We hypothesize that platelet impairment of the ADP pathway correlates with fibrinolysis sensitivity in trauma patients. METHODS: A prospective observational study of patients meeting the criteria for the highest level of activation at an urban trauma center was performed. Viscoelastic parameters associated with platelet function (maximum amplitude [MA]) were measured with native thrombelastography (TEG), and TEG platelet mapping of the ADP pathway (ADP-MA). The contribution of fibrinogen to clotting was measured with TEG (angle) and the TEG functional fibrinogen (FF) assay (FF-MA). Another TEG assay containing tissue-type plasminogen activator (t-PA) (75 ng mL(-1) ) was used to assess clot sensitivity to an exogenous fibrinolytic stimulus by use of the TEG lysis at 30 min (LY30) variable. Multivariate linear regression was used to identify which TEG variable correlated with t-PA-LY30 (quantification of fibrinolysis sensitivity). RESULTS: Fifty-eight trauma patients were included in the analysis, with a median injury severity score of 17 and a base deficit of 6 mEq L(-1) . TEG parameters that significantly predicted t-PA-LY30 were related to platelet function (ADP-MA, P = 0.001; MA, P < 0.001) but not to fibrinogen (FF-MA, P = 0.773; angle, P = 0.083). Clinical predictors of platelet ADP impairment included calcium level (P = 0.001), base deficit (P = 0.001), and injury severity (P = 0.001). RESULTS AND CONCLUSIONS: Platelet impairment of the ADP pathway is associated with increased sensitivity to t-PA. ADP pathway inhibition in platelets may be an early step in the pathogenesis of systemic hyperfibrinolysis.

Process of care and outcomes for elderly patients hospitalized with peptic ulcer disease: results from a quality improvement project.

CONTEXT: Since publication in 1994 of guidelines for management of peptic ulcer disease (PUD), trends in physician practice and outcomes related to guideline application have not been evaluated. OBJECTIVES: To describe changes in process of care that occurred in a quality improvement program for patients hospitalized with PUD and to evaluate associations between in-hospital treatment of PUD and 1-year rehospitalization for PUD and mortality in a subset of these patients. DESIGN, SETTING, AND PATIENTS: Cohort study of 4292 sequential Medicare beneficiaries hospitalized at acute care hospitals with a principal diagnosis of PUD in 5 states (Colorado, Georgia, Connecticut, Oklahoma, and Virginia) in 1995 (baseline) and 1997 (remeasurement); outcomes were evaluated for 752 patients in Colorado. MAIN OUTCOME MEASURES: Changes in rates of screening for Helicobacter pylori infection, treatment for H pylori infection, screening for nonsteroidal anti-inflammatory drug (NSAID) use, counseling about NSAID use; outcomes included rehospitalization for PUD and all-cause mortality within 1 year of discharge in Colorado. RESULTS: Screening for H pylori infection increased significantly (12%-19% increase; P<.001) in each of the 5 states. Treatment of H pylori infection increased in each state and was significantly increased for the entire group of hospitalizations examined (8% increase overall; P =.001). Despite increased screening, detection of H pylori infection was less frequent than expected in every state, (13%-24%) and did not increase in any state. Screening for and counseling about NSAIDs did not significantly increase overall or in any state. In the Colorado cohort, the proportion of patients rehospitalized was unchanged in 1995 (8.9%) and 1997 (6.8%), and 124 patients (16%) in the combined 1995 and 1997 cohorts died within 1 year. Treatment for H pylori was not associated with a reduction in rehospitalization within 1 year (adjusted odds ratio [OR], 1.24; 95% confidence interval [CI], 0.65-2.36) or with a reduction in mortality (adjusted OR, 1.08; 95% CI, 0.68-1.71). Counseling about NSAID use was associated with a decrease in risk of 1-year rehospitalization for PUD (adjusted OR, 0.47; 95% CI, 0.22-0.99) and risk of all-cause mortality (adjusted OR, 0.44; 95% CI, 0.26-0.75). CONCLUSIONS: This quality improvement program for elderly patients with PUD resulted in increased screening for H pylori and increased treatment of H pylori infection but no change in counseling about NSAID use. However, with the low prevalence of H pylori detected, treatment of H pylori infection was not associated with a reduction in repeat hospitalization for PUD or subsequent mortality, whereas counseling about the risks of using NSAIDs was associated with a reduction in the risk of both outcomes.

Influencing care in acute myocardial infarction: a randomized trial comparing 2 types of intervention.

The purpose of this study was to evaluate performance feedback delivered by on-site presentations compared to mailed feedback on improving acute myocardial infarction (AMI) care. We used a randomized trial including 18 hospitals nested within the Cooperative Cardiovascular Project. Patients comprised AMI Medicare patients admitted before (n = 929, 1994 and 1995) and after intervention (n = 438, 1996). Control hospitals received written feedback by mail. The experimental intervention group received a presentation led by a cardiologist and a quality improvement specialist. We assessed the proportion of patients receiving appropriate AMI care before and after the intervention. Both univariate and multivariate analyses demonstrated no effect of the intervention in increasing the proportion of patients who received reperfusion, aspirin, beta-blockers, or angiotensin-converting enzyme inhibitors. On-site feedback presentations were not associated with a larger improvement in AMI care compared to the mailed feedback. Other interventions, such as opinion leaders and patient-directed interventions, may be necessary in order to improve the care of AMI patients.

Serologic testing for inflammatory bowel disease.

OBJECTIVES: To determine the accuracy of anti-neutrophil cytoplasmic antibodies (ANCAs) and anti-Saccharomyces cerevisiae antibodies (ASCA) in distinguishing patients with inflammatory bowel disease from patients with other disorders, seen in a pediatric gastroenterology clinic setting, and in distinguishing ulcerative colitis (UC) from Crohn's disease (CD). STUDY DESIGN: Serum samples from 120 children with new or established diagnoses of UC (n = 25) or CD (n = 20) and control children (n = 74) were analyzed in blinded fashion for the presence of IgG ANCAs and IgA and IgG ASCA. RESULTS: The highest sensitivity for detecting inflammatory bowel disease, 71%, was achieved by using ANCAs and ASCA together. The best test for UC was ANCAs, which had a sensitivity of 80%. However, the ANCA pattern characteristic of UC, perinuclear ANCAs eliminated by DNAse, had a sensitivity of 60%. High-titer ANCAs were specific for UC, whereas ASCA were specific for CD. CONCLUSIONS: Testing for ANCAs and ASCA together did not achieve sensitivity necessary for population screening. However, ANCAs and ASCA may be helpful in evaluating children suspected of having inflammatory bowel disease and in distinguishing UC from CD.

Symptomatic colonic polyps in childhood: not so benign.

BACKGROUND: The clinical spectrum of symptomatic polyps and the frequency of familial polyposis is not well defined in children. In the present study, a series of children with juvenile polyposis coli (JPC) and non-JPC polyps were studied. METHODS: Children with symptomatic colonic polyps and negative family history of polyps were ascertained by review of endoscopic records. Juvenile polyposis coli was defined as 10 or more juvenile polyps or any juvenile polyp in a relative of an index case of JPC. Polyps were tested for Ki-ras mutations, p53 overexpression, and aneuploidy. RESULTS: Seventy-eight children (age range, 0.4-18 years) were identified, all evaluated for lower gastrointestinal bleeding. Nine (12%) had JPC, 66 (84%) had isolated juvenile polyps, and 3 (4%) had other types of polyps. The JPC and non-JPC groups were similar in age (p = 0.4) and symptom duration (p = 0.3). The JPC group had more polyps (p = 0.0001), and greater likelihood of anemia (p = 0.01), polyps with adenomatous change (p = 0.03), and right-colon polyps (p = 0.001). In three of eight JPC families, polyps were identified in asymptomatic first-degree relatives. No abnormalities in Ki-ras, p53, or aneuploidy were identified. CONCLUSIONS: Juvenile polyposis coli is common in children with symptomatic polyps, and is associated with anemia, right-colon polyps, and adenomas. The risk of polyps and of colorectal cancer in relatives of persons with JPC requires further study.

Increasing influenza and pneumococcal vaccination and tuberculosis screening among residents of Colorado long-term care facilities.

Persons residing in long-term care facilities are especially vulnerable to potentially preventable morbidity and mortality caused by influenza, S. pneumoniae, and tuberculosis. This project's objective was to increase the rates of pneumococcal vaccination, tuberculosis screening, and annual influenza vaccination. Intervention consisted of staff training videos, sample policies, and educational materials for residents and their families. At baseline during the 1995-1996 flu season, 84% of Colorado long-term care residents were vaccinated for influenza; 16% of residents had ever received pneumococcal vaccination; and 59% had been screened for tuberculosis. At remeasurement during 1997 to 1998, influenza vaccination rates were up to 89%, p = 0.006. The percentage of residents who had ever received pneumococcal vaccination increased to 48% at remeasurement, p < 0.001. Tuberculosis screening rates increased to 83%, p < 0.001. Following an educational intervention targeting both residents and staff, residents were significantly more likely to receive all three preventive services.

Autologous blood transfusion does not reduce postoperative infection rates in elective surgery.

BACKGROUND: The influence of blood transfusions in the risk of postoperative infection remains controversial. We examined the association between autologous (AB) and homologous (HB) blood transfusions with postoperative infection in elective surgery. METHODS: The medical records of 991 Medicare patients aged > or =65 years submitted to hysterectomy and hip and knee replacement were reviewed. Logistic regression analysis was used to control for age, comorbidity, year, and type of procedure. RESULTS: Overall, 451 (46%) patients required transfusions. AB was given to 324 (72%), HB to 94 (21%); 33 (7%) patients received both. Forty-two patients (4%) developed postoperative infections. The infection rate was not different among patients receiving HB (7%), AB (5%), AB+HB (0), and nontransfused patients (4%); P = 0.18). After adjustment for confounders, HB and AB remained not associated with infections. CONCLUSION: In elective surgery with small volume transfusion, neither AB nor HB transfusions were associated with an increased risk of postoperative infections.

Multiple organ failure can be predicted as early as 12 hours after injury.

BACKGROUND: The failure of therapies aimed at modulating systemic inflammatory response syndrome and decreasing multiple organ failure (MOF) has been attributed in part to the inability to identify early the population at risk. Our objective, therefore, was to develop predictive models for MOF at admission and at 12, 24 and 48 hours after injury. METHODS: Logistic regression models were derived in a data set with 411 adult trauma patients using indicators of tissue injury, shock, host factors, and the Acute Physiology Score-Acute Physiology and Chronic Health Evaluation III (APS-APACHE III). RESULTS: MOF was diagnosed in 78 patients (19%). Injury Severity Score, platelet count, and age emerged as predictors in all models. Transfused blood, inotropes, and lactate were significant predictors at 12, 24, and 48 hours, but not at admission. The APS-APACHE III emerged only in the 0- to 48-hour model and offered minimal improvement in predictive power. Good predictive power was achieved at 12 hours after injury. CONCLUSION: Postinjury MOF can be predicted as early as 12 hours after injury. The APS-APACHE III added little to the predictive power of tissue injury, shock and host factors.

Secretory phospholipase A2 cleavage of intravasated bone marrow primes human neutrophils.

BACKGROUND: Recent clinical reports suggest that early femoral intramedullary rod (IMR) fixation in patients with multiple injuries increases the risk of adult respiratory distress syndrome (ARDS). We have shown that lipid-mediated neutrophil (PMN) priming and elevated circulating levels of secretory phospholipase A2 (sPLA2) within the first 24 hours after injury correlate with the development of ARDS. We thus hypothesized that circulating lipid products, generated by sPLA2 cleavage of intravasated bone marrow, prime PMNs for enhanced superoxide anion (O2-) production. METHODS: Isolated PMNs from healthy volunteers were incubated for 5 minutes with buffer or sPLA2-lysed bone marrow (100 U/mL) collected from trauma patients. After formyl-methionyleucylphenylalanine (fMLP) activation, O2- production was quantified by the superoxide dismutase-inhibitable reduction of cytochrome c. Blood samples were also drawn from five injured patients before and 24 hours after femoral IMR fixation. PMNs were isolated and assessed for in vivo priming. RESULTS: PMNs incubated with sPLA2-lysed bone marrow were primed for more than 3.5 times greater fMLP-induced O2- production. Furthermore, in patients with femoral fractures, PMN O2- release in response to fMLP after IMR fixation was more than 2.5 times higher than before fixation. CONCLUSION: Collectively, the findings suggest that bone marrow released from acute fracture sites may become a lipid substrate for the elevated sPLA2 levels found in injured patients. The resultant priming of PMNs may thus render the injured patient at risk for ARDS. Although clearly hypothetical at present, we submit that these observations warrant further investigation because of their clinical implications.

Prospective characterization and selective management of the abdominal compartment syndrome.

BACKGROUND: The abdominal compartment syndrome (ACS) is now recognized as a frequent confounder of surgical critical care following major trauma; however, few prospective data exist concerning its characterization, evolution, and response to decompression. METHODS: Acutely injured patients with an injury severity scale (ISS) score >15 requiring emergent laparotomy and intensive care unit (ICU) admission were prospectively evaluated for the development of ACS. The syndrome was defined as an intra-abdominal pressure (IAP) >20 mm Hg complicated by one of the following: peak airway pressure (PAP) >40 cm H2O, oxygen delivery index (DO2I) <600 mL O2/min/m2, or urine output (UO) <0.5 mL/kg/hr. Physiologic response to decompression was similarly documented prospectively. RESULTS: Over a 14-month period ending December 1995, 21 (14%) of 145 patients (ISS >15) requiring laparotomy and admitted to our surgical ICU developed ACS; mean age was 39 +/- 9 years; injury mechanism was blunt in 60%; ISS 26 +/- 6. At initial laparotomy, 67% underwent abdominal packing (57% for major liver injuries). Mean IAP was 27 +/- 2.3 mm Hg, and time from laparotomy to decompression was 27 +/- 4 hours; 24% were planned whereas the remaining were prompted by deteriorating organ function as defined above (cardiopulmonary in 43%; renal in 19%; both renal and cardiopulmonary in 14%). Following decompression, there was an increase in cardiac index, oxygen delivery, urine output, and static compliance while there was a decrease in pulmonary capillary wedge pressure, systemic vascular resistance, and peak airway pressure. CONCLUSIONS: The abdominal compartment syndrome occurs in a significant number of severely injured patients, and it develops quickly (27 +/- 4 hours). Cardiopulmonary deterioration is the most frequent reason prompting decompression. Timely decompression of the ACS results in improvements in cardiopulmonary and renal function. These data support the use of the proposed ACS grading system for selective management of the syndrome.

Blood transfusion. An independent risk factor for postinjury multiple organ failure.

OBJECTIVE: To determine if blood transfusion is a consistent risk factor for postinjury multiple organ failure (MOF), independent of other shock indexes. DESIGN: A 55-month inception cohort study ending on August 30, 1995. Data characterizing postinjury MOF were prospectively collected. Multiple logistic regression analysis was performed on 5 sets of data. Set 1 included admission data (age, sex, comorbidity, injury mechanism, Glasgow Coma Scale, Injury Severity Score, and systolic blood pressure determined in the emergency department) plus the amount of blood transfused within the first 12 hours. In the subsequent 4 data sets, other indexes of shock (early base deficit, early lactate level, late base deficit, and late lactate level) were sequentially added. Additionally, the same multiple logistic regression analyses were performed with early MOF and late MOF as the outcome variables. SETTING: Denver General Hospital, Denver, Colo, is a regional level I trauma center. PATIENTS: Five hundred thirteen consecutive trauma patients admitted to the trauma intensive care unit with an Injury Severity Score greater than 15 who were older than 16 years and who survived longer than 48 hours. INTERVENTIONS: None. MAIN OUTCOME MEASURES: The relationship of blood transfusions and other shock indexes with the outcome variable, MOF. RESULTS: A dose-response relationship between early blood transfusion and the later development of MOF was identified. Despite the inclusion of other indexes of shock, blood transfusion was identified as an independent risk factor in 13 of the 15 multiple logistic regression models tested; the odds ratios were high, especially in the early MOF models. CONCLUSIONS: Blood transfusion is an early consistent risk factor for postinjury MOF, independent of other indexes of shock.

Predicting life-threatening coagulopathy in the massively transfused trauma patient: hypothermia and acidoses revisited.

BACKGROUND: Recalcitrant coagulopathy "the bloody vicious cycle," produces the majority of deaths after torso trauma. A model predicting this life-threatening complication may facilitate clinical decision-making. METHODS: We prospectively analyzed patients > 15 years old who received a massive transfusion (> 10 units of packed red blood cells (PRBC)/24 h) over a 2-year period. Excluding massive head injuries and pre-existing disease, the 58 study patients had a mean age = 35.4 years, Injury Severity Score (ISS) = 30.6, and PRBC = 24.2 units/24 h. RESULTS: Defined as prothrombin time of two times that of normal laboratory controls and partial thromboplastin time as two times that of normal laboratory controls, 27 patients (47%) developed life-threatening coagulopathy. Using a multiple logistic regression model, the four significant risk factors (with odds ratio) were (1) pH < 7.10 (12.3), (2) temperature < 34 degrees C (8.7), (3) ISS > 25 (7.7), and (4) systolic blood pressure < 70 mm Hg (5.8). The conditional probability of developing coagulopathy was ISS > 25 + systolic blood pressure < 70 mm Hg = 39%, ISS > 25 + temperature < 34 degrees C = 49%, ISS > 25 + pH < 7.10 = 49%; with all four risk factors the incidence was 98%. CONCLUSION: Postinjury life-threatening coagulopathy in the seriously injured requiring massive transfusion is predicted by persistent hypothermia and progressive metabolic acidosis.

Jack A. Barney Resident Research Award winner. The inflammatory profile of interleukin-6, interleukin-8, and soluble intercellular adhesion molecule-1 in postinjury multiple organ failure.

BACKGROUND: Interleukin-6 (IL-6), interleukin-8 (IL-8), and adhesion molecules have been implicated as mediators in neutrophil (PMN) and endothelial cell (EC) interactions leading to postinjury multiple organ failure (MOF). Our hypothesis was that circulating levels of IL-6, IL-8, and soluble intercellular adhesion molecule-1 (sICAM-1) would discriminate patients at risk for postinjury MOF. METHODS: Serial plasma levels of IL-6, IL-8, and sICAM-1 were measured in 27 high-risk trauma patients. RESULTS: The IL-6 and IL-8 levels were significantly elevated in MOF patients compared with non-MOF patients at 12 and 36 hours postinjury. The IL-6 level was also elevated at 84 and 132 hours, and IL-8 at 84 hours. The sICAM-1 level did not become elevated in MOF patients until 132 hours postinjury. CONCLUSION: Interleukin-6 and IL-8 are elevated early after trauma and discriminate patients who will develop MOF. Late elevation of sICAM-1 likely results from PMN cytotoxicity leading to EC injury or inflammation.

Early risk factors for postinjury multiple organ failure.

Epidemiologic studies, based on retrospective data from heterogeneous populations with poor control of confounders, led early investigators to conclude that infection was the overriding risk factor for multiple organ failure (MOF). More recent studies have convincingly shown that MOF frequently occurs in the absence of infection. Consequently, we have shifted our research focus away from the traditional infectious models of MOF to the newer "one-hit" and "two-hit" inflammatory models. Clinically, we have chosen to study trauma patients because they are a relatively homogeneous group with a low incidence of common confounders. Trauma also permits a clear distinction between the first insult and the outcome, both temporally and with respect to the definition criteria. In this review we discuss the background, rationale, and our initial attempts to use indicators of the first insult (i.e., tissue injury quantification and clinical signs of shock) and indicators of the host response (i.e., systemic inflammatory response syndrome) to predict MOF early after injury.

Postinjury multiple organ failure: a bimodal phenomenon.

To better define the epidemiology of postinjury multiple organ failure (MOF), we prospectively evaluated 457 high-risk trauma patients who survived more than 48 hours. Overall, 70 (15%) developed MOF. In 27 (39%) patients, the occurrence was early, while in 43 (61%) patients the presentation was delayed. At presentation, early MOF had more cardiac dysfunction, while late MOF had greater hepatic failure. Indices of shock were more critical risk factors for early MOF, while advanced age was more important for late MOF. While early and late MOF had a similar high incidence of major infections, these appeared to be more important in precipitating late MOF. Finally, while mortality is similar, early MOF patients appear to succumb faster. In conclusion, postinjury MOF remains a significant challenge and appears to present in at least two patterns (i.e., early versus late). Better understanding of the relative roles of the dysfunctional inflammation and infections in early MOF versus late MOF may facilitate the development of new strategies for the prevention and treatment of morbid syndrome.

Early neutrophil sequestration after injury: a pathogenic mechanism for multiple organ failure.

Polymorphonuclear neutrophils (PMNs) play a pivotal role in the inflammation that precedes multiple organ failure (MOF). In a rat model of MOF, PMNs become primed for enhanced superoxide anion (O2-) release and CD11b expression, sequester in end organs, and produce organ failure. Therefore, we hypothesized that circulating PMNs harvested in the first 24 hours after injury from trauma patients at risk for MOF would (1) exhibit a primed O2- release, (2) upregulate CD11b expression, and (3) show evidence of sequestration in tissues. Extracellular PMN O2- release and CD11b receptor expression were measured at 3, 6, 12, and 24 hours after injury in 33 torso trauma patients with Injury Severity Scores > 15; eight patients (24%) developed MOF. Healthy adults served as controls. PMNs after injury were primed for enhanced in vitro O2- release at 3, 6, 12, and 24 hours after injury, indicating prior in vivo priming. CD11b expression was also increased at 6, 12, and 24 hours after injury. Circulating PMN numbers increased sharply at 3 hours after injury, before decreasing dramatically at 6 and 12 hours, suggesting end organ sequestration. At 12 hours after injury, declines in circulating PMNs were significantly greater in MOF than in non-MOF patients (p < 0.05). These data indicate that PMNs are quickly mobilized into the circulation after injury and then primed for enhanced O2- release and CD11b expression. PMN priming appears to be a necessary preamble to PMN sequestration in patients with major torso trauma. Upregulation of PMN function, accompanied by subsequent end organ sequestration, may represent an important early event in the pathogenesis of MOF after injury.

Epidemiology of trauma deaths: a reassessment.

OBJECTIVE: 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. DESIGN: Cross-sectional. MATERIAL AND METHODS: 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. MEASUREMENTS AND MAIN RESULTS: 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%). CONCLUSIONS: 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.

Extrapleural bupivacaine for amelioration of multiple rib fracture pain.

OBJECTIVE: The pain associated with multiple rib fractures can be surprisingly variable. The objective of this study was to determine the efficacy of an indwelling, percutaneously placed intercostal catheter in relieving the pain associated with multiple rib fractures. DESIGN: Prospective nonrandomized study setting: Surgical intensive care unit in a level 1 trauma center. SUBJECTS: Fifteen blunt chest trauma patients with a minimum of three rib fractures who had failed an intravenous patient controlled analgesia protocol. INTERVENTIONS: Insertion of an epidural catheter within the intercostal space. Bupivacaine 0.25% with epinephrine was injected in a volume of 20 mL. Subsequent doses were limited to a total of 400 mg per 24 hours. MEASUREMENTS AND MAIN RESULTS: Severity of injury was estimated by using the Injury Severity Score. For each patient a preinjection visual analogue scale (VAS) and incentive spirometry (IS) lung volume were determined. Fifteen minutes following injection of 0.25% bupivacaine with epinephrine the VAS and IS were repeated. The Injury Severity Score ranged from 9 to 32 (mean 19.0 +/- 1.6). Overall, mean VAS pain scores improved significantly following the initial bolus of bupivacaine (before VAS = 7.5 +/- 0.6, after VAS = 3.5 +/- 0.5, p < 0.05) and this was associated with significant increase in IS lung volumes (before IS = 0.77 +/- 0.09, after IS = 1.3 +/- 0.13, p < 0.05). No patient experienced either insertion-related or drug administration complications. CONCLUSIONS: These results confirm that an indwelling intercostal catheter provides a continuous nerve block resulting in a simple, safe procedure that can ameliorate the pain and splinting associated with multiple rib fractures. Although we experienced no complications, additional investigation is clearly needed.

Cardiac enzymes are irrelevant in the patient with suspected myocardial contusion.

BACKGROUND: Myocardial contusion is commonly diagnosed following blunt chest trauma, and has potentially lethal complications. Cost-effective case management in patients with suspected myocardial contusion is confounded by the low incidence of complications and the lack of a reliable test to predict them. The clinical usefulness of elevated cardiac enzyme levels is controversial. METHODS: We analyzed a 4-year experience of 359 patients with high-risk blunt chest trauma who were assessed using an established practice guideline. Our multivariate statistical model evaluated all of the early risk factors included in the guideline, specifically focusing on cardiac enzyme levels. RESULTS: Myocardial contusion was diagnosed in 30% of patients, and complications (dysrhythmias and cardiogenic shock) occurred in 5%. In no case was cardiac enzyme elevation the sole predictor of a complication. The cost of routine cardiac enzyme assay was substantial. CONCLUSION: Cardiac enzyme determinations have no useful role in the evaluation of patients with suspected myocardial contusion. They should be eliminated from current practice guidelines.