Potential use of biochar, compost and iron grit associated with Trifolium repens to stabilize Pb and As on a multi-contaminated technosol.

Vegetation cover can be used in the phytomanagement of polluted areas by adding value to abandoned sites and reducing the dispersion of pollutants by erosion. Appropriate amendments, that allow both efficient plant growth and the immobilization of contaminants in the soil must be chosen in order to optimize the efficiency of this process. We used a mining technosol mainly contaminated by arsenic (1068 mg kg-1) and lead (23387 mg kg-1) to study the effect of three amendments (biochar, compost and iron grit) on (i) physico-chemical properties of the soil and soil pore water, (ii) metal(loid) mobility, bioavailability and bioaccessibility (CaCl2 and Simple Bioaccessibility Extraction Test (SBET)), and (iii) the capability of Trifolium repens to germinate and grow. All the amendments used increased the pH and electrical conductivity of the SPW, resulting in a 90% decrease in the concentration of lead in the soil pore water (SPW). We also demonstrated a decrease in Pb phytoavailability. The amendments allowed the establishment of a plant cover, although the addition of iron grit alone did not allow any clover germination. For the Pontgibaud technosol, the combination of the three amendments resulted in a significant decrease in As and Pb concentrations in clover tissues, mainly in the aerial organs. The amendments also made it possible for some of them to halve the phytoavailable fraction of arsenic. However, for compost, both the As concentrations in the SPW, and the bioavailable fraction of As increased. All the amendments used had contrasting effects on the bioaccessible fractions of metal(loid)s. The most efficient amendment combination was the addition of 5% biochar and 5% compost.

Capability of amendments (biochar, compost and garden soil) added to a mining technosol contaminated by Pb and As to allow poplar seed (Populus nigra L.) germination.

The germination capacity of poplar seeds has never been studied in the context of metal(loid)-contaminated soils, even though poplars are present over a vast geographical area. In this study, black poplar seeds from the Loire Valley (France) were grown for 28 days in mesocosm on a heavily polluted soil that was subjected to different amendments. This phytomanagement process aimed to allow the revegetation of an As and Pb-contaminated mining soil by adding appropriate amendments, resulting in metal(loid) soil stabilisation and efficient plant growth. The objectives were to evaluate the effect of three amendments (garden soil, compost and biochar) when added alone or combined to a technosol on (i) the soil physicochemical properties, (ii) the mobility of As and Pb in the soil pore water (SPW), (iii) the capacity of poplar seeds to germinate and to grow and (iv) the metal(loid) distribution within the plant organs. The addition of amendments alone or combined allowed a 90% decrease in SPW Pb concentrations, while the arsenic concentrations were between 18 and 416 times higher. However, we were only able to obtain seed germination and plant growth on amended soils. These promising results will allow us to explore the use of such amendments in rehabilitating areas that are sources of significant metal(loid) dissemination, as well as allowing a natural plant recolonisation of these sites by seeds from the surrounding environment.

Impaired glucose metabolism in the heart of obese Zucker rats after treatment with phorbol ester.

OBJECTIVE: To investigate the influence of obesity on the regulation of myocardial glucose metabolism following protein kinase C (PKC) activation in obese (fa/fa) and lean (Fa/?) Zucker rats. DESIGN: Isolated hearts obtained from 17-week-old lean and obese Zucker rats were perfused with 200 nM phorbol 12-myristate 13-acetate (PMA) for different time periods prior to the evaluation of PKC and GLUT-4 translocation. For metabolic studies isolated hearts from 48 h starved Zucker rats were perfused with an erythrocytes-enriched buffer containing increased concentrations (10-100 nM) of PMA. MEASUREMENTS: Immunodetectable PKC isozymes and GLUT-4 were determined by Western blots. Glucose oxidation and glycolysis were evaluated by measuring the myocardial release of 14CO2 and 3H2O from [U-14C]glucose and [5-3H]glucose, respectively. RESULTS: PMA (200 nM) induced maximal translocation of ventricular PKCalpha from the cytosol to the membranes within 10 min. This translocation was 2-fold lower in the heart from obese rats when compared to lean rats. PMA also induced a significant translocation of ventricular GLUT-4 from the microsomal to the sarcolemmal fraction within 60 min in lean but not in obese rats. Rates of basal cardiac glucose oxidation and glycolysis in obese rats were approximately 2-fold lower than those of lean rats. Perfusion with increasing concentrations of PMA (10-100 nM) led to a significant decrease of cardiac glucose oxidation in lean but not in obese rats. CONCLUSION: Our results show that in the heart of the genetically obese Zucker rat, the impairment in PKCalpha activation is in line with a diminished activation of GLUT-4 as well as with the lack of PMA effect on glucose oxidation.

Hypotension, hypoxia, and head injury: frequency, duration, and consequences.

BACKGROUND: Retrospective studies have suggested an association between systemic hypotension and hypoxia and worsened outcome from traumatic brain injury. Little is known, however, about the frequency and duration of these potentially preventable causes of secondary brain injury. HYPOTHESIS: Early episodes of hypoxia and hypotension occurring during initial resuscitation will have a significant impact on outcome following traumatic brain injury. DESIGN: Prospective cohort study. SETTING: Urban level I trauma center. PATIENTS: Patients with a traumatic brain injury who had a Glasgow Coma Score of 12 or less within the first 24 hours of admission to the hospital and computed tomographic scan results demonstrating intracranial pathologic features. Patients who died in the emergency department were excluded from the study. MAIN OUTCOME MEASURES: Automated blood pressure and pulse oximetry readings were collected prospectively from the time of arrival through initial resuscitation. The number and duration of hypotensive (systolic blood pressure, < or =90 mm Hg) and hypoxic (oxygen saturation, < or =92%) events were analyzed for their association with mortality and neurological outcome. RESULTS: One hundred seven patients met the enrollment criteria (median Glasgow Coma Score, 7). Overall mortality was 43%. Twenty-six patients (24%) had hypotension while in the emergency department, with an average of 1.5 episodes per patient (mean duration, 9.1 minutes). Of these 26 patients with hypotension, 17 (65%) died (P =.01). When the number of hypotensive episodes increased from 1 to 2 or more, the odds ratio for death increased from 2.1 to 8.1. Forty-one patients (38%) had hypoxia, with an average of 2.1 episodes per patient (mean duration, 8.7 minutes). Of these 41 patients with hypoxia, 18 (44%) died (P =.68). CONCLUSIONS: Hypotension, but not hypoxia, occurring in the initial phase of resuscitation is significantly (P =.009) associated with increased mortality following brain injury, even when episodes are relatively short. These prospective data reinforce the need for early continuous monitoring and improved treatment of hypotension in brain-injured patients.

Obesity is associated with impaired ventricular protein kinase C-MAP kinase signaling and altered ANP mRNA expression in the heart of adult Zucker rats.

BACKGROUND: In the obesity model of the Zucker rat, myocardial protein kinase C (PKC) activation by phorbol ester is impaired. The influence of obesity on myocardial cell signaling was investigated by studying the activation of PKC isozymes and MAP kinases (MAPK) p38 and p42/44 as well as the induction of ANP mRNA. METHODS: Isolated hearts obtained from 17-week-old lean and obese Zucker rats were perfused with 200 nM phorbol 12-myristate 13-acetate (PMA) at different time periods. Immunodetectable PKC isozymes, phosphorylated-MAPK, and ANP mRNA were determined by Western and Northern blots, respectively. RESULTS: PMA promoted a marked transient translocation of ventricular PKCalpha from the cytosol to the membranes within 10 minutes in lean rats, whereas it had a much weaker effect in obese rats. Moreover, PMA induced a significant activation of PKCdelta in lean but not in obese rat hearts. After PKC activation, increases in phosphorylation levels of myocardial p38 and p42 MAPK were approximately 3-fold higher in lean rats than in obese animals. Concerning the induction of ANP, PMA transiently tripled ANP mRNA within 60 minutes in lean but not in obese rats. CONCLUSIONS: In the genetically obese Zucker rat, the myocardial signal transduction cascade PKC-MAPK-ANP mRNA seems to be markedly impaired. It can be speculated that this abnormal cardiac cell signaling in obese rats reflects an early phase in the cardiac pathogenesis accompanying obesity.

Carbon dioxide reactivity and pressure autoregulation of brain tissue oxygen.

OBJECTIVE: To describe the normal relationships between brain tissue oxygen tension (PbrO2) and physiological parameters of systemic blood pressure and CO2 concentrations. METHODS: Licox Clark-type oxygen probes (GMS mbH, Kiel, Germany) were inserted in the frontal white matter of 12 swine maintained under general anesthesia with a 1.0 fraction of inspired oxygen (FiO2). In seven swine, alterations in end-tidal carbon dioxide (ET-CO2) concentration (range, 13-72 mm Hg) were induced via hyperventilation or instillation of CO2 into the ventilation circuit. In nine swine, mean arterial pressure (MAP) (range, 33-200 mm Hg) was altered; phenylephrine was used to induce hypertension, and a nitroprusside-esmolol combination or systemic hemorrhage was used for hypotension. Quantitative cerebral blood flow (CBF) was measured in two animals by using a thermal diffusion probe. RESULTS: Mean baseline PbrO2 was 41.9 +/- 11.3 mm Hg. PbrO2 varied linearly with changes in ET-CO2, ranging from 20 to 60 mm Hg (r2 = 0.70). The minimum PbrO2 with hypocarbia was 5.9 mm Hg, and the maximum PbrO2 with hypercarbia was 132.4 mm Hg. PbrO2 varied with MAP in a sigmoid fashion suggestive of pressure autoregulation between 60 and 150 mm Hg (r2 = 0.72). The minimum PbrO2 with hypotension was 1.4 mm Hg, and the maximum PbrO2 with hypertension was 97.2 mm Hg. In addition, CBF correlated linearly with PbrO2 during CO2 reactivity testing (r2 = 0.84). CONCLUSION: In the uninjured brain, PbrO2 exhibits CO2 reactivity and pressure autoregulation. The relationship of PbrO2 with ET-CO2 and MAP appears to be similar to those historically established for CBF with ET-CO2 and MAP. This suggests that, under normal conditions, PbrO2 is strongly influenced by factors that regulate CBF.

The effects of pressure control versus volume control assisted ventilation on patient work of breathing in acute lung injury and acute respiratory distress syndrome.

BACKGROUND: Patient work of breathing (WOB) during assisted ventilation is reduced when inspiratory flow (V(I)) from the ventilator exceeds patient flow demand. Patients in acute respiratory failure often have unstable breathing patterns and their requirements for V(I) may change from breath to breath. Volume control ventilation (VCV) traditionally incorporates a pre-set ventilator V(I) that remains constant even under conditions of changing patient flow demand. In contrast, pressure control ventilation (PCV) incorporates a variable decelerating flow wave form with a high ventilator V(I) as inspiration commences. We compared the effects of flow patterns on assisted WOB during VCV and PCV. METHODS: WOB was measured with a BICORE CP-100 monitor (incorporating a Campbell Diagram) in a prospective, randomized cross-over study of 18 mechanically ventilated adult patients with acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). Tidal volume, inspiratory time, and mean ventilator V(I) were constant in each mode. RESULTS: At comparable levels of respiratory drive and minute ventilation, patient WOB was significantly lower with PCV than with VCV (0.59 +/- 0.42 J/L vs 0.70 +/- 0.58 J/L, respectively, p < 0.05). Ventilator peak V(I) was significantly higher with PCV than with VCV (103.2 +/- 22.8 L/min vs 43.8 L/min, respectively, p < 0.01). CONCLUSIONS: In the setting of ALI and ARDS, PCV significantly reduced patient WOB relative to VCV. The decrease in patient WOB was attributed to the higher ventilator peak V(I) of PCV.

Cerebral oxygenation during hemorrhagic shock: perils of hyperventilation and the therapeutic potential of hypoventilation.

OBJECTIVES: Prophylactic hyperventilation of patients with head injuries worsens outcome, presumably by exacerbating tissue hypoxia. Oxygen tension in brain tissue (PbrO2) provides a direct measurement of cerebral metabolic substrate delivery and varies with changing end-tidal carbon dioxide tension (ETCO2) and mean arterial pressure. However, the effects of hyperventilation and hypoventilation on PbrO2 during hemorrhagic shock are not known. The aim of this study was to examine the effects of alteration in ventilation on PbrO2 in hemorrhaged swine. METHODS: Clark-type polarographic probes were inserted into the brain tissue of seven swine to measure PbrO2 directly. To examine the effects of alterations in ventilation on hemorrhage-induced hypotension, swine were hemorrhaged to 50% estimated blood volume and PbrO2 was monitored during hyperventilation (RR = 30) and hypoventilation (RR = 4). RESULTS: After the 50% hemorrhage, PbrO2 declined rapidly from 39.8 +/- 4.6 mm Hg to 11.4 +/- 2.2 mm Hg. Hyperventilation resulted in a further 56% mean decrease in PbrO2. Hypoventilation produced a 166% mean increase in PbrO2. These changes were significant (p = 0.001) for absolute and percentage differences from baseline. CONCLUSION: During hemorrhage, alterations in ventilation significantly changed PbrO2: hyperventilation increased brain-tissue hypoxia whereas hypoventilation alleviated it. This finding suggests that hyperventilation has deleterious effects on brain oxygenation in patients with hemorrhagic shock and those with head trauma. Conversely, hypoventilation with resultant hypercapnia may actually help resolve hemorrhagic shock-induced cerebral hypoxia.

Initial severity of metabolic acidosis predicts the development of acute lung injury in severely traumatized patients.

OBJECTIVES: First, to determine whether the severity of shock, as measured by systemic hypotension and metabolic acidosis, is significantly associated with a higher risk of acute lung injury in patients with severe trauma. Second, to determine whether the volumes of blood and crystalloid solutions administered in the early posttrauma period are independent risk factors for acute lung injury in severely traumatized patients. DESIGN: Prospective observational study. SETTING: Level I urban trauma center in a university hospital. PATIENTS: A total of 102 severely injured, mechanically ventilated trauma patients with an Injury Severity Score > or =16 and aged between 18 and 75 yrs. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Initial clinical and laboratory data were collected in the emergency department, and on a daily basis thereafter during the patient's intensive care unit stay. Of the 102 severely injured patients enrolled, 42 developed acute lung injury (41%) and 60 did not (59%). A total of 93% of the trauma patients who developed acute lung injury during the 17-month study period were included in the study. Initial base deficit was significantly lower in patients who developed acute lung injury than in those who did not (-8.8+/-4.5 vs. -5.6+/-5.1, p<.01). The difference in systolic blood pressure between the two groups was not significant. CONCLUSIONS: In this group of severely injured trauma patients, the degree of metabolic acidosis at the time of admission identified those patients with the highest probability of developing acute lung injury. In addition, the volume of crystalloid solution administered during the first 24 hrs was significantly greater in patients who later developed acute lung injury. Finally, there was a significantly higher morbidity in patients who developed acute lung injury, whereas mortality did not differ between the two groups.

Role of cell contractions in cAMP-induced cardiomyocyte atrial natriuretic peptide release.

Incubation of spontaneously beating ventricular cardiomyocytes from neonatal rats with prostaglandin E(2) (0.1 microM) or forskolin (0.1 microM) simultaneously increased the rate of cellular contraction and atrial natriuretic peptide (ANP) secretion. Both responses were maximal within 10-20 min of application and were accompanied by three- to fourfold increases in cAMP formation. By contrast, a higher regimen of forskolin (10 microM) promoted a 20- to 30-fold increase in basal cAMP production, which was accompanied by the abolition of contractile activity and ANP release. Low regimens of forskolin (0.1 microM) doubled the occurrence of cytosolic Ca(2+) transients associated with monolayer contraction, whereas higher regimens of forskolin (10 microM) completely suppressed Ca(2+) transients. Moreover, in quiescent cultures that were pretreated with ryanodine, tetrodotoxin, nifedipine, or butanedione monoxime, prostaglandin E(2) (0.1 microM) and forskolin (0.1 microM) failed to elicit significant ANP secretion, suggesting that cAMP-elevating agents promote ANP secretion to a great extent via an increase in cellular contraction frequency in ventricular cardiomyocytes.

Leukocytosis and free fluid are important indicators of isolated intestinal injury after blunt trauma.

BACKGROUND: The detection of isolated intestinal injuries after blunt trauma can be difficult because of subtle signs and symptoms, often leading to delayed diagnosis. We hypothesized that specific clinical indicators could be identified to assist in the diagnosis of these injuries. METHODS: Medical records of all patients with such injuries from 1988 to 1996 were reviewed. The patients were stratified into those operated on within 6 hours of presentation (apparent injury) and those operated on after 6 hours (occult injury), and the data were compared. RESULTS: Forty-six patients with isolated intestinal injuries were identified. There were no differences in the rate of peritonitis or free fluid on abdominal computed tomography, blood loss, intraoperative findings, or morbidity and mortality between groups. Leukocytosis (sensitivity, 84.8%; specificity, 55.2%; p = 0.01) and free fluid on computed tomography were frequently present, however, and their significance was underappreciated in the occult injury group. CONCLUSION: After blunt abdominal trauma in patients without obvious indications for invasive evaluation of the abdomen (e.g., peritoneal lavage, laparoscopy, laparotomy), leukocytosis can indicate an intestinal injury. Additionally, unexplained free fluid on abdominal computed tomography must be aggressively evaluated.

Brain tissue oxygenation during hemorrhagic shock, resuscitation, and alterations in ventilation.

OBJECTIVES: Recently developed polarographic microelectrodes permit continuous, reliable monitoring of oxygen tension in brain tissue (PbrO2). The aim of this study was to investigate the feasibility and utility of directly monitoring PbrO2 in cerebral tissue during changes in oxygenation or ventilation and during hemorrhagic shock and resuscitation. We also sought to develop a model in which treatment protocols could be evaluated using PbrO2 as an end point. METHODS: Licox Clark-type polarographic probes were inserted in the brain tissue of 16 swine to monitor PbrO2. In eight swine, changes in PbrO2 were observed over a range of fractional concentrations of inspired O2 (FiO2) as well as during periods of hyperventilation and hypoventilation. In eight other swine, PbrO2 was monitored during a graded hemorrhage of up to 70% estimated blood volume and during the resuscitation period. RESULTS: When FiO2 was elevated to 100%, PbrO2 increased from a baseline of 15+/-2 mm Hg to 36+/-11 mm Hg. Hyperventilation while breathing 100% oxygen resulted in a 40% decrease in PbrO2 (p < 0.05), whereas hypoventilation increased PbrO2 to 88 mm Hg (p < 0.01). A graded hemorrhage to 50% estimated blood volume significantly reduced PbrO2, mean arterial pressure, and intracranial pressure (p < 0.01). Continued hemorrhage to 70% estimated blood volume resulted in a PbrO2 of 2.9+/-1.5 mm Hg. After resuscitation, PbrO2 was significantly elevated, reaching 65+/-13 mm Hg (p < 0.01), whereas mean arterial pressure and cerebral perfusion pressure simply returned to baseline. CONCLUSION: Directly measured PbrO2 was highly responsive to changes in FiO2, ventilatory rate, and blood volume in this experimental model. In particular, hypoventilation significantly increased PbrO2, whereas hyperventilation had the opposite effect. The postresuscitation increase in PbrO2 may reflect changes in both O2 delivery and O2 metabolism. These experiments set the stage for future investigations of a variety of resuscitation protocols in both normal and injured brain.

Fasciotomy, chronic venous insufficiency, and the calf muscle pump.

OBJECTIVE: To test the hypothesis that fasciotomy may impair the function of the calf muscle pump, which in turn could result in the development of chronic venous insufficiency. DESIGN: A cohort study of patients with a history of lower extremity fasciotomy. SETTING: An urban trauma center. PATIENTS: Seventeen of the 83 patients identified through trauma, vascular, and/or orthopedic registries consented to participation in this study. INTERVENTIONS: Participating patients completed a study questionnaire, and then underwent a complete vascular examination, including air plethysmographic (APG) assessment. Patients with a history of venous injuries were also studied with color flow duplex venous imaging. MAIN OUTCOME MEASURES: Function of the calf muscle pump as measured by APG, and evidence of chronic venous insufficiency as measured by APG, findings on clinical examination, and by venous ultrasonography. RESULTS: Seventeen patients completed the study, including 8 with a history of vascular injuries, 6 with old fractures, and 3 who had undergone fasciotomy for soft tissue infections. The time from injury to examination ranged from 5 months to 20 years. Eight patients had signs or symptoms of venous insufficiency, the severity of which appeared to be time dependent. The APG data showed significant mean differences between fasciotomy and control extremities in ejection fraction (P<.001) and residual volume fraction (P<.001), both measures of calf muscle pump function. There were no significant changes in venous filling index, a measure of venous reflux, or in outflow fraction, which correlates with venous obstruction. There were no differences in APG variables between patients with vascular injuries vs those with orthopedic or soft tissue injuries. CONCLUSIONS: Lower extremity fasciotomy impairs long-term calf muscle pump function, as measured by APG, in patients with and without vascular injuries. These patients are at risk for the long-term development of chronic venous insufficiency following lower extremity trauma.

Role of cAMP and calcium influx in endothelin-1-induced ANP release in rat cardiomyocytes.

The mechanism of endothelin-1 (ET-1)-induced atrial natriuretic peptide (ANP) release was studied in neonatal rat ventricular cardiomyocytes. These cells expressed a single high-affinity class of ETA receptor (dissociation constant = 54 +/- 18 pM, n = 3), but no ETB receptors. Incubation of cardiomyocytes with ET-1 led to concentration-dependent ANP release and prostacyclin production. ET-1-induced ANP release was affected by neither protein kinase C (PKC) inhibition or downregulation nor by cyclooxygenase inhibition, indicating that ET-1-stimulated ANP secretion is not a PKC-mediated, prostaglandin-dependent process. Furthermore, ET-1 significantly stimulated adenosine 3',5'-cyclic monophosphate (cAMP) production and increased cytosolic calcium concentration in these preparations. Both ET-1-induced calcium influx and ANP release were decreased by the cAMP antagonist Rp-cAMPS, the Rp diastereoisomer of cAMP. Moreover, ET-1-induced ANP secretion was strongly inhibited in the presence of nifedipine as well as in the absence of extracellular calcium. Thus our results suggest that ET-1 stimulates ANP release in ventricular cardiomyocytes via an ETA receptor-mediated pathway involving cAMP formation and activation of a nifedipine-sensitive calcium channel.

Use of tissue oxygen tension measurements during resuscitation from hemorrhagic shock.

BACKGROUND: Tissue oxygen tension can be measured directly in selected organ beds, and these measurements may be more sensitive in assessing the adequacy of resuscitation than global physiologic parameters. We hypothesized that heart tissue oxygen tension would be an important marker for the severity of ischemic insult to the heart during hemorrhagic shock. We further hypothesized that gut oxygen tension measured in the jejunum would prove to be a better measure of splanchnic hypoperfusion than intramucosal pH (pHi). METHODS: Tissue oxygen probes were inserted directly into the myocardium of the left ventricle and into the lumen of the proximal jejunum in 10 anesthetized swine. A pHi catheter was introduced into the stomach. The animals were subjected to a controlled hemorrhage of 50% of estimated blood volume. Gut and cardiac oxygen were monitored continuously during hemorrhage and resuscitation, which was performed with shed blood and crystalloid. RESULTS: While gut O2 and pHi trended together, we were unable to establish a correlation between changes in these two variables during hemorrhage and resuscitation. Heart PO2 decreased significantly during hemorrhage, but surpassed baseline values after resuscitation, a finding not seen in gut PO2. No standard physiologic variables reliably predicted changes in heart PO2 during these experiments. CONCLUSIONS: Tissue oxygen tensions measurements are highly responsive to changes induced during graded hemorrhagic shock and resuscitation. Gut PO2 and pHi appear to be measuring different physiologic processes in the gastrointestinal tract. The compensatory ability of the heart far exceeds that of the gut after ischemic insult. This hemorrhagic shock model appears feasible for the study of various methods of resuscitation.

Use of low molecular weight heparin in preventing thromboembolism in trauma patients.

OBJECTIVE: To investigate the safety and effectiveness of low molecular weight heparin (LMWH) in preventing deep venous thrombosis (DVT) in high-risk trauma patients, compared with mechanical methods of prophylaxis. DESIGN: A prospective randomized trial conducted over a 19-month period in an urban, academic trauma center. METHODS: All trauma patients with the following risk factors for the development of DVT were considered for enrollment in this study: any injury with an Abbreviated Injury Scale score > or = 3; major head injury (Glasgow Coma Scale score < or = 8); spine, pelvic, or lower extremity fractures; acute venous injury; or age > 50 years. After a screening venous duplex examination, the patients were assigned to a Heparin versus No-Heparin group, depending upon the presence of injuries precluding the use of heparin. In the Heparin group, the patients were then randomized to receive either LMWH or optimal mechanical compression (defined as bilateral sequential gradient pneumatic compression (SCD) or, in the presence of lower extremity injuries precluding the use of the SCD, the arteriovenous impulse (AVI) compression system). All the patients in the No-Heparin group received optimal compression. Enrolled patients underwent sequential duplex examinations every 5 to 7 days until discharge. RESULTS: Of the 487 consecutive patients initially enrolled in this study, 372 were available for at least the first two duplex examinations and comprise the study population. Only nine (2.4%) patients developed DVT, compared with the predicted 9.1% rate in high-risk trauma patients receiving no prophylaxis (p = 0.037). Of the 120 patients who were randomized to receive LMWH, only one (0.8%) developed DVT. In the SCD group, there were 5 of 199 patients (2.5%) with DVT, and 3 of 53 (5.7%) in the AVI group. One patient with DVT also had clinical symptoms of pulmonary embolism, but there were no deaths secondary to pulmonary embolism. There was one major bleeding complication potentially associated with the use of LMWH. CONCLUSIONS: The administration of LMWH is a safe and extremely effective method of preventing DVT in high-risk trauma patients. When heparin is contraindicated, aggressive attempts at mechanical compression are warranted.

Trauma experience of Navy surgeons: assessment and commentary.

Numerous reports have suggested that surgical readiness during Operation Desert Storm was poor. We surveyed active duty Navy surgeons to assess current trauma experience and capability. A survey concerning trauma and critical care experience, as well as self-rating of skills, was mailed to all active duty surgeons (n = 185) in 1993. The response rate was 79% (146/185). A high turnover rate of surgeons was indicated by: (1) 51% (75/146) of surgeons had less than 3 years of experience following residency; and (2) only 42% (61/146) had served in the Gulf War. Only 12% of active duty surgeons (18/146) were involved in trauma care. Only 10% (14/146) had performed more than 20 operations for trauma in the preceding 1 years, and 85% (124/146) had performed fewer than 10 operations. In the preceding 5 years, 84% (122/146) had performed fewer than 100 operations for trauma, and 42% (61/146) had performed none. Critical care experience ranged from 0 to 20 patients per month (mean = 3). Despite limited recent experience, 84% (123/146) of respondents rated their trauma skills as adequate (n = 43), good (n = 49), or excellent (n = 31). We conclude that most Navy surgeons have minimal recent experience in trauma care. A high rate of turnover mandates training strategies that provide an ongoing exposure to injured patients. This could be accomplished by designating military hospitals as trauma centers or by placing military surgeons in civilian trauma centers.