Pub Date : 2009-01-01DOI: 10.1097/TA.0b013e318156835c
Y. Kosashvili, D. Backstein, Y. B. Ziv, O. Safir, A. Blumenfeld, Y. Mirovsky
INTRODUCTION Backboards are routinely used to protect the spine of trauma patients during transportation. Nevertheless, little is known about the biomechanical properties of this type of immobilization. OBJECTIVES To evaluate the mechanical support of the thoracolumbosacral spine provided by a standard backboard in comparison with various rigid immobilization surfaces, by examining their respective surface contact area (SCA). MATERIALS SCAs comparisons of a standard aluminum backboard, a rigid military stretcher, an aluminum backboard covered by blanket, 3 and 5 cm thickness foam, and a cushioned stretcher were made using 12 volunteers. The evaluation was performed by a computer- mediated system that generated a diagram indicating pressure distribution and SCA score in each volunteer. These data were compared with a medical grade mattress, which served as the control group. RESULTS The median backboard's SCA was 14.6 +/- 5.5 times smaller than the stretcher's SCA (range 4.6-28, average 15, p < 0.001). Its median SCA was essentially doubled by covering it by a standard military blanket and tripled when covered by 3 cm layer of foam. Using a 5-cm layer of foam increased the backboard's SCA by 11 times. Cushioning the stretcher beneath the lumbar spine and the hamstrings by folded blankets, significantly improved its median SCA (96 +/- 31.1, range 36-125, average 89.7). CONCLUSIONS The backboard's SCA was significantly inferior to all the other surfaces. Although no dynamic evaluation was performed, these data imply that backboards need to be appropriately cushioned or alternate surfaces should be employed to improve the mechanical support during trauma patient transportation. Level of evidence, Level I.
{"title":"A biomechanical comparison between the thoracolumbosacral surface contact area (SCA) of a standard backboard with other rigid immobilization surfaces.","authors":"Y. Kosashvili, D. Backstein, Y. B. Ziv, O. Safir, A. Blumenfeld, Y. Mirovsky","doi":"10.1097/TA.0b013e318156835c","DOIUrl":"https://doi.org/10.1097/TA.0b013e318156835c","url":null,"abstract":"INTRODUCTION Backboards are routinely used to protect the spine of trauma patients during transportation. Nevertheless, little is known about the biomechanical properties of this type of immobilization. OBJECTIVES To evaluate the mechanical support of the thoracolumbosacral spine provided by a standard backboard in comparison with various rigid immobilization surfaces, by examining their respective surface contact area (SCA). MATERIALS SCAs comparisons of a standard aluminum backboard, a rigid military stretcher, an aluminum backboard covered by blanket, 3 and 5 cm thickness foam, and a cushioned stretcher were made using 12 volunteers. The evaluation was performed by a computer- mediated system that generated a diagram indicating pressure distribution and SCA score in each volunteer. These data were compared with a medical grade mattress, which served as the control group. RESULTS The median backboard's SCA was 14.6 +/- 5.5 times smaller than the stretcher's SCA (range 4.6-28, average 15, p < 0.001). Its median SCA was essentially doubled by covering it by a standard military blanket and tripled when covered by 3 cm layer of foam. Using a 5-cm layer of foam increased the backboard's SCA by 11 times. Cushioning the stretcher beneath the lumbar spine and the hamstrings by folded blankets, significantly improved its median SCA (96 +/- 31.1, range 36-125, average 89.7). CONCLUSIONS The backboard's SCA was significantly inferior to all the other surfaces. Although no dynamic evaluation was performed, these data imply that backboards need to be appropriately cushioned or alternate surfaces should be employed to improve the mechanical support during trauma patient transportation. Level of evidence, Level I.","PeriodicalId":92962,"journal":{"name":"The journal of cardiothoracic trauma","volume":"23 4 1","pages":"191-4"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83577344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-01-01DOI: 10.1097/TA.0b013e318191bfe0
L. Rael, R. Bar-Or, D. Ambruso, C. Mains, D. Slone, M. Craun, D. Bar-Or
BACKGROUND Transfusion-related acute lung injury (TRALI) is a life-threatening condition characterized by oxidative stress. Longer storage times of packed red blood cells (PRBC) and other blood products have been implicated with an increased risk in developing TRALI in transfused patients. METHODS A total of 10 units of blood containing PRBC stored in citrate-phosphate-dextrose buffer at 4 degrees C were included in the study. At Bonfils Blood Center (Denver, CO), samples were collected on storage day 1 and day 42. Samples were immediately centrifuged, and the supernatants were collected and stored at -80 degrees C until further analysis. Oxidation-reduction potential and protein oxidation were measured in both the day 1 and day 42 samples. RESULTS Oxidation-reduction potential significantly increased (p < 0.05) in the day 42 sample (98.1 mV +/- 21.9 SD) versus the day 1 sample (62.6 mV +/- 21.5 SD). The oxidation of human serum albumin increased by 63.6% during the storage time. Other serum proteins such as apolipoprotein A1 and transthyretin demonstrated similar increases in oxidation. Also, proteins with a cleaved C-terminal amino acid were observed indicating the presence of carboxypeptidase activity, a marker of inflammation. CONCLUSIONS The presence of an oxidative environment in transfused PRBC increases with storage time. This could partially explain the increased risk of developing TRALI related to the transfusion of older blood products.
{"title":"The effect of storage on the accumulation of oxidative biomarkers in donated packed red blood cells.","authors":"L. Rael, R. Bar-Or, D. Ambruso, C. Mains, D. Slone, M. Craun, D. Bar-Or","doi":"10.1097/TA.0b013e318191bfe0","DOIUrl":"https://doi.org/10.1097/TA.0b013e318191bfe0","url":null,"abstract":"BACKGROUND Transfusion-related acute lung injury (TRALI) is a life-threatening condition characterized by oxidative stress. Longer storage times of packed red blood cells (PRBC) and other blood products have been implicated with an increased risk in developing TRALI in transfused patients. METHODS A total of 10 units of blood containing PRBC stored in citrate-phosphate-dextrose buffer at 4 degrees C were included in the study. At Bonfils Blood Center (Denver, CO), samples were collected on storage day 1 and day 42. Samples were immediately centrifuged, and the supernatants were collected and stored at -80 degrees C until further analysis. Oxidation-reduction potential and protein oxidation were measured in both the day 1 and day 42 samples. RESULTS Oxidation-reduction potential significantly increased (p < 0.05) in the day 42 sample (98.1 mV +/- 21.9 SD) versus the day 1 sample (62.6 mV +/- 21.5 SD). The oxidation of human serum albumin increased by 63.6% during the storage time. Other serum proteins such as apolipoprotein A1 and transthyretin demonstrated similar increases in oxidation. Also, proteins with a cleaved C-terminal amino acid were observed indicating the presence of carboxypeptidase activity, a marker of inflammation. CONCLUSIONS The presence of an oxidative environment in transfused PRBC increases with storage time. This could partially explain the increased risk of developing TRALI related to the transfusion of older blood products.","PeriodicalId":92962,"journal":{"name":"The journal of cardiothoracic trauma","volume":"1 1","pages":"76-81"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83595845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-01-01DOI: 10.1097/TA.0b013e3181938c5e
N. Mowery, O. Gunter, Oscar D. Guillamondegui, Lesly A. Dossett, Marcus J. Dortch, John A. Morris, A. May
BACKGROUND Both hyper- and hypoglycemia have been associated with poor outcome in traumatic brain injury (TBI). Neither the risks nor benefit of tight glucose control (goal range, 80-110 mg/dL) have been documented in the TBI population. OBJECTIVE To analyze whether densely collected blood glucose data, using a computerized algorithm, to maintain tight glycemic control will reveal significant differences in blood glucose control between survivors and nonsurvivors in patients with TBI. METHODS From October 2005 to April 2006, all ventilated, critically ill surgical patients with TBI Abbreviated Injury Scale score of >or=3 were placed on an automated, euglycemia protocol with every 2-hour blood glucose sampling. Mortalities within 24 hours were excluded. The protocol calculates the insulin rate using a linear equation (rate = blood glucose - 60[M]). M is an adapting multiplier and used here as a marker for insulin resistance (IR). RESULTS Of 1,636 trauma intensive care unit admissions 160 patients, (median Injury Severity Score 34, mortality 13.1%) had 10,071 samples collected. Median glucose 115.6 mg/dL, with 41% of values between 80 and 110 mg/dL, 81% between 80 and 150 mg/dL, and 0.3% <40 mg/dL. The median blood glucose was statistically different but not clinically different among the patients who lived and died (114; interquartile range, 109-132 vs. 118; 111-136, p = 0.01). The median insulin dose was a unit per hour higher among the patient who died (4.2; 2.7-5.9 vs. 3.2; 2.4-5.0, p = 0.006). A logistic regression model demonstrated insulin rate (odds ratio 0.736, 95% confidence interval, 0.549-0.985, p = 0.039) to be the only independent predictor of mortality among the measures of blood glucose control. CONCLUSION Nonsurvivors with TBI have significantly higher markers of IR (insulin rate and multiplier). Markers of glucose control (median glucose, hypoglycemic episodes, and the percentage of values in range) did not differ clinically among groups. Despite this stress IR, tight glycemic control appears possible and safe with low levels of hypoglycemic episodes in the TBI population.
背景:高血糖和低血糖都与创伤性脑损伤(TBI)的不良预后相关。严格控制血糖(目标范围80-110 mg/dL)的风险和益处在TBI人群中都没有记录。目的:分析采用计算机化算法密集收集血糖数据以维持严格的血糖控制是否会揭示TBI患者幸存者和非幸存者之间血糖控制的显着差异。方法2005年10月至2006年4月，所有TBI简易损伤量表评分>或=3分的通气危重外科患者均采用自动血糖测定方案，每2小时采集一次血糖。不包括24小时内的死亡率。该方案使用线性方程计算胰岛素率(率=血糖- 60[M])。M是一种自适应乘数，在这里用作胰岛素抵抗(IR)的标记。结果在1636例外伤重症监护病房入院的160例患者中(损伤严重程度评分中位数为34，死亡率为13.1%)采集了10071份样本。葡萄糖中位数为115.6 mg/dL，其中41%在80 - 110 mg/dL之间，81%在80 - 150 mg/dL之间，0.3% <40 mg/dL。生存和死亡患者的中位血糖有统计学差异，但无临床差异(114;四分位数范围，109-132 vs. 118;111 ~ 136, p = 0.01)。死亡患者的中位胰岛素剂量每小时高1个单位(4.2;2.7-5.9 vs. 3.2;2.4 ~ 5.0, p = 0.006)。logistic回归模型显示胰岛素率(优势比0.736,95%可信区间0.549-0.985,p = 0.039)是血糖控制指标中唯一的独立预测因子。结论创伤性脑损伤非幸存者的IR指标(胰岛素率和乘数)明显升高。血糖控制指标(中位数血糖、低血糖发作和范围内值的百分比)在组间没有临床差异。尽管有这种应激性IR，但在TBI人群中，严格的血糖控制对于低血糖发作的低水平来说是可能和安全的。
{"title":"Stress insulin resistance is a marker for mortality in traumatic brain injury.","authors":"N. Mowery, O. Gunter, Oscar D. Guillamondegui, Lesly A. Dossett, Marcus J. Dortch, John A. Morris, A. May","doi":"10.1097/TA.0b013e3181938c5e","DOIUrl":"https://doi.org/10.1097/TA.0b013e3181938c5e","url":null,"abstract":"BACKGROUND Both hyper- and hypoglycemia have been associated with poor outcome in traumatic brain injury (TBI). Neither the risks nor benefit of tight glucose control (goal range, 80-110 mg/dL) have been documented in the TBI population. OBJECTIVE To analyze whether densely collected blood glucose data, using a computerized algorithm, to maintain tight glycemic control will reveal significant differences in blood glucose control between survivors and nonsurvivors in patients with TBI. METHODS From October 2005 to April 2006, all ventilated, critically ill surgical patients with TBI Abbreviated Injury Scale score of >or=3 were placed on an automated, euglycemia protocol with every 2-hour blood glucose sampling. Mortalities within 24 hours were excluded. The protocol calculates the insulin rate using a linear equation (rate = blood glucose - 60[M]). M is an adapting multiplier and used here as a marker for insulin resistance (IR). RESULTS Of 1,636 trauma intensive care unit admissions 160 patients, (median Injury Severity Score 34, mortality 13.1%) had 10,071 samples collected. Median glucose 115.6 mg/dL, with 41% of values between 80 and 110 mg/dL, 81% between 80 and 150 mg/dL, and 0.3% <40 mg/dL. The median blood glucose was statistically different but not clinically different among the patients who lived and died (114; interquartile range, 109-132 vs. 118; 111-136, p = 0.01). The median insulin dose was a unit per hour higher among the patient who died (4.2; 2.7-5.9 vs. 3.2; 2.4-5.0, p = 0.006). A logistic regression model demonstrated insulin rate (odds ratio 0.736, 95% confidence interval, 0.549-0.985, p = 0.039) to be the only independent predictor of mortality among the measures of blood glucose control. CONCLUSION Nonsurvivors with TBI have significantly higher markers of IR (insulin rate and multiplier). Markers of glucose control (median glucose, hypoglycemic episodes, and the percentage of values in range) did not differ clinically among groups. Despite this stress IR, tight glycemic control appears possible and safe with low levels of hypoglycemic episodes in the TBI population.","PeriodicalId":92962,"journal":{"name":"The journal of cardiothoracic trauma","volume":"5 1","pages":"145-51; discussion 151-3"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89254795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-01-01DOI: 10.1097/TA.0b013e318190c3a1
R. Friese, Brandon R. Bruns, C. Sinton
BACKGROUND Sleep deprivation is a common problem in the intensive care unit. Animal models have demonstrated that sleep deprivation alone is associated with increased mortality. We have previously shown that septic insult with sleep deprivation results in increased mortality in a murine model. The aging process is known to reduce the restorative phases of sleep. The purpose of this study was to evaluate the effect of age on mortality with sleep deprivation during recovery from septic insult. METHODS C57BL/6J male mice aged 2 months (young) or 9 months (old) underwent cecal ligation and puncture (CLP). Animals were randomized to receive sleep interruption (SI) for 48 hours or standard recovery (no SI). Sham animals underwent laparotomy and cecal manipulation without puncture. SI was achieved by securing animal housing to an orbital shaker set to repeatedly cycle at 30 rpm over 120 seconds (30 seconds on/90 seconds off). The primary outcome was survival at 5 days post-CLP. Kaplan-Meier survival analysis with log-rank test was used to explore differences in mortality. RESULTS SI resulted in an increase in time awake for both light and dark cycles (p < 0.001). Mortality after CLP with SI (n = 30) was 57% and mortality after CLP without SI (controls; n = 33) was 24%. SI was associated with a greater than 3-fold increase in mortality after CLP (RR = 3.29; 95% CI, 1.42-7.63). Young mice (n = 28) had a mortality of 31% with CLP alone increasing to 67% with SI (p = 0.03). Old mice (n = 35) had a mortality of 18% with CLP alone increasing to 50% with SI (p = 0.05). There was no difference in survival between young and old mice undergoing SI (p = 0.49). CONCLUSIONS Sleep deprivation after septic insult increases mortality in both young and old mice. However, sleep deprivation after septic insult does not have a more profound effect on mortality in either age group. These findings suggest that sleep deprivation experienced in the intensive care unit setting during recovery from critical illness may increase mortality. This effect appears independent of increased age. Further studies evaluating extremes of age are warranted.
{"title":"Sleep deprivation after septic insult increases mortality independent of age.","authors":"R. Friese, Brandon R. Bruns, C. Sinton","doi":"10.1097/TA.0b013e318190c3a1","DOIUrl":"https://doi.org/10.1097/TA.0b013e318190c3a1","url":null,"abstract":"BACKGROUND Sleep deprivation is a common problem in the intensive care unit. Animal models have demonstrated that sleep deprivation alone is associated with increased mortality. We have previously shown that septic insult with sleep deprivation results in increased mortality in a murine model. The aging process is known to reduce the restorative phases of sleep. The purpose of this study was to evaluate the effect of age on mortality with sleep deprivation during recovery from septic insult. METHODS C57BL/6J male mice aged 2 months (young) or 9 months (old) underwent cecal ligation and puncture (CLP). Animals were randomized to receive sleep interruption (SI) for 48 hours or standard recovery (no SI). Sham animals underwent laparotomy and cecal manipulation without puncture. SI was achieved by securing animal housing to an orbital shaker set to repeatedly cycle at 30 rpm over 120 seconds (30 seconds on/90 seconds off). The primary outcome was survival at 5 days post-CLP. Kaplan-Meier survival analysis with log-rank test was used to explore differences in mortality. RESULTS SI resulted in an increase in time awake for both light and dark cycles (p < 0.001). Mortality after CLP with SI (n = 30) was 57% and mortality after CLP without SI (controls; n = 33) was 24%. SI was associated with a greater than 3-fold increase in mortality after CLP (RR = 3.29; 95% CI, 1.42-7.63). Young mice (n = 28) had a mortality of 31% with CLP alone increasing to 67% with SI (p = 0.03). Old mice (n = 35) had a mortality of 18% with CLP alone increasing to 50% with SI (p = 0.05). There was no difference in survival between young and old mice undergoing SI (p = 0.49). CONCLUSIONS Sleep deprivation after septic insult increases mortality in both young and old mice. However, sleep deprivation after septic insult does not have a more profound effect on mortality in either age group. These findings suggest that sleep deprivation experienced in the intensive care unit setting during recovery from critical illness may increase mortality. This effect appears independent of increased age. Further studies evaluating extremes of age are warranted.","PeriodicalId":92962,"journal":{"name":"The journal of cardiothoracic trauma","volume":"55 1","pages":"50-4"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80066002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-01-01DOI: 10.1097/TA.0b013e31819313bb
B. Cotton, B. Au, T. Nunez, O. Gunter, A. Robertson, P. Young
INTRODUCTION Massive transfusion (MT) protocols have been shown to improve survival in severely injured patients. However, others have noted that these higher fresh frozen plasma (FFP):red blood cell (RBC) ratios are associated with increased risk of organ failure. The purpose of this study was to determine whether MT protocols are associated with increased organ failure and complications. METHODS Our institution's exsanguination protocol (TEP) involves the immediate delivery of products in a 3:2 ratio of RBC:FFP and 5:1 for RBC:platelets. All patients receiving TEP between February 2006 and January 2008 were compared with a cohort (pre-TEP) of all patients from February 2004 to January 2006 that (1) went immediately to the operating room and (2) received MT (>or=10 units of RBC in first 24 hours). RESULTS Two hundred sixty-four patients met inclusion (125 in the TEP group, 141 in the pre-TEP). Demographics and Injury Severity Score were similar. TEP received more intraoperative FFP and platelets but less in first 24 hours (p < 0.01). There was no difference in renal failure or systemic inflammatory response syndrome, but pneumonia, pulmonary failure, open abdomens, and abdominal compartment syndrome were lower in TEP. In addition, severe sepsis or septic shock and multiorgan failure were both lower in the TEP patients (9% vs. 20%, p = 0.011 and 16% vs. 37%, p < 0.001, respectively). CONCLUSIONS Although MT has been associated with higher organ failure and complication rates, this risk appears to be reduced when blood products are delivered early in the resuscitation through a predefined protocol. Our institution's TEP was associated with a reduction in multiorgan failure and infectious complications, as well as an increase in ventilator-free days. In addition, implementation of this protocol was followed by a dramatic reduction in development of abdominal compartment syndrome and the incidence of open abdomens.
{"title":"Predefined massive transfusion protocols are associated with a reduction in organ failure and postinjury complications.","authors":"B. Cotton, B. Au, T. Nunez, O. Gunter, A. Robertson, P. Young","doi":"10.1097/TA.0b013e31819313bb","DOIUrl":"https://doi.org/10.1097/TA.0b013e31819313bb","url":null,"abstract":"INTRODUCTION Massive transfusion (MT) protocols have been shown to improve survival in severely injured patients. However, others have noted that these higher fresh frozen plasma (FFP):red blood cell (RBC) ratios are associated with increased risk of organ failure. The purpose of this study was to determine whether MT protocols are associated with increased organ failure and complications. METHODS Our institution's exsanguination protocol (TEP) involves the immediate delivery of products in a 3:2 ratio of RBC:FFP and 5:1 for RBC:platelets. All patients receiving TEP between February 2006 and January 2008 were compared with a cohort (pre-TEP) of all patients from February 2004 to January 2006 that (1) went immediately to the operating room and (2) received MT (>or=10 units of RBC in first 24 hours). RESULTS Two hundred sixty-four patients met inclusion (125 in the TEP group, 141 in the pre-TEP). Demographics and Injury Severity Score were similar. TEP received more intraoperative FFP and platelets but less in first 24 hours (p < 0.01). There was no difference in renal failure or systemic inflammatory response syndrome, but pneumonia, pulmonary failure, open abdomens, and abdominal compartment syndrome were lower in TEP. In addition, severe sepsis or septic shock and multiorgan failure were both lower in the TEP patients (9% vs. 20%, p = 0.011 and 16% vs. 37%, p < 0.001, respectively). CONCLUSIONS Although MT has been associated with higher organ failure and complication rates, this risk appears to be reduced when blood products are delivered early in the resuscitation through a predefined protocol. Our institution's TEP was associated with a reduction in multiorgan failure and infectious complications, as well as an increase in ventilator-free days. In addition, implementation of this protocol was followed by a dramatic reduction in development of abdominal compartment syndrome and the incidence of open abdomens.","PeriodicalId":92962,"journal":{"name":"The journal of cardiothoracic trauma","volume":"39 1","pages":"41-8; discussion 48-9"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77933316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-01-01DOI: 10.1097/TA.0b013e318193109b
H. Azuma, S. Mishima, J. Oda, H. Homma, H. Sasaki, M. Hisamura, S. Ohta, T. Yukioka
BACKGROUND Normal gut flora plays an important role in the intestinal mucosal barrier function under various critical conditions. The flora may alter after severe insults, such as trauma and shock. Enteral nutrition should preserve the gut environment; however, full support is usually difficult for severely ill patients because of impaired gastrointestinal motility. Currently, we have commercial enteral supplementation product enriched with glutamine, dietary fiber, and oligosaccharide (GFO) in Japan. This study examines the hypothesis that the enteral supplementation ameliorates gut injury induced by a bacterial overgrowth model, even in small volumes and quantities. MATERIALS Balb/c mice received antibiotics (4 mg/mL of streptomycin) in their drinking water for 4 days to kill the normal gut flora after which they were orally inoculated with a streptomycin-resistant strain of Escherichia coli, known as E. coli C-25. The mice that were administered bacterial monoassociation received 0.5 mL of GFO twice daily (GFO group) or 10% of glucose solution (GLU group). Unsupplemented drinking water was used for control animals (control) whose gut flora was normal. The mice were killed and their mesenteric lymph nodes complex was harvested and processed to test gut bacterial translocation. The cecal population levels of bacteria and ileum histology were also examined. RESULTS The incidence and magnitude of gut translocation to the lymph nodes complex in the GLU group were significantly higher than those in the control (p < 0.01). Treatment with GFO prevented the gut translocation although animals in the GFO group had same level of the cecal bacterial population. Histologic findings in the ileum were not different between the GLU and GFO. CONCLUSION GFOs supplement prevented gut translocation for bacterial overgrowth even in small volumes and quantities. The intestinal histologic findings could not explain the protective mechanisms of GFO. Further studies may be needed to elucidate the benefit of the partial enteral nutrition.
背景正常肠道菌群在肠黏膜屏障功能中发挥重要作用。在严重的伤害，如创伤和休克后，菌群可能发生改变。肠内营养应保护肠道环境;然而，由于胃肠运动功能受损，重症患者通常难以获得完全的支持。目前，我们在日本有富含谷氨酰胺、膳食纤维和低聚糖(GFO)的肠内补充产品。本研究检验了肠内补充改善细菌过度生长模型引起的肠道损伤的假设，即使是小体积和数量。在balb /c小鼠的饮用水中加入抗生素(4 mg/mL链霉素)4天，以杀死正常肠道菌群，之后口服接种耐链霉素的大肠杆菌菌株，称为大肠杆菌c -25。给予细菌单关联的小鼠每天两次给予0.5 mL GFO (GFO组)或10%葡萄糖溶液(GLU组)。肠道菌群正常的对照组(对照)采用不补充饮用水。小鼠被杀死，它们的肠系膜淋巴结复合体被收集并处理以测试肠道细菌易位。还检查了盲肠菌群水平和回肠组织学。结果GLU组患者肠易位至淋巴结复合物的发生率和程度均显著高于对照组(p < 0.01)。尽管GFO组动物的盲肠细菌数量相同，但GFO治疗可防止肠道易位。回肠的组织学表现在GLU和GFO之间没有差异。结论即使小剂量和小剂量补充fos也能防止肠道细菌过度生长的易位。肠道组织学结果不能解释GFO的保护机制。可能需要进一步的研究来阐明部分肠内营养的益处。
{"title":"Enteral supplementation enriched with glutamine, fiber, and oligosaccharide prevents gut translocation in a bacterial overgrowth model.","authors":"H. Azuma, S. Mishima, J. Oda, H. Homma, H. Sasaki, M. Hisamura, S. Ohta, T. Yukioka","doi":"10.1097/TA.0b013e318193109b","DOIUrl":"https://doi.org/10.1097/TA.0b013e318193109b","url":null,"abstract":"BACKGROUND Normal gut flora plays an important role in the intestinal mucosal barrier function under various critical conditions. The flora may alter after severe insults, such as trauma and shock. Enteral nutrition should preserve the gut environment; however, full support is usually difficult for severely ill patients because of impaired gastrointestinal motility. Currently, we have commercial enteral supplementation product enriched with glutamine, dietary fiber, and oligosaccharide (GFO) in Japan. This study examines the hypothesis that the enteral supplementation ameliorates gut injury induced by a bacterial overgrowth model, even in small volumes and quantities. MATERIALS Balb/c mice received antibiotics (4 mg/mL of streptomycin) in their drinking water for 4 days to kill the normal gut flora after which they were orally inoculated with a streptomycin-resistant strain of Escherichia coli, known as E. coli C-25. The mice that were administered bacterial monoassociation received 0.5 mL of GFO twice daily (GFO group) or 10% of glucose solution (GLU group). Unsupplemented drinking water was used for control animals (control) whose gut flora was normal. The mice were killed and their mesenteric lymph nodes complex was harvested and processed to test gut bacterial translocation. The cecal population levels of bacteria and ileum histology were also examined. RESULTS The incidence and magnitude of gut translocation to the lymph nodes complex in the GLU group were significantly higher than those in the control (p < 0.01). Treatment with GFO prevented the gut translocation although animals in the GFO group had same level of the cecal bacterial population. Histologic findings in the ileum were not different between the GLU and GFO. CONCLUSION GFOs supplement prevented gut translocation for bacterial overgrowth even in small volumes and quantities. The intestinal histologic findings could not explain the protective mechanisms of GFO. Further studies may be needed to elucidate the benefit of the partial enteral nutrition.","PeriodicalId":92962,"journal":{"name":"The journal of cardiothoracic trauma","volume":"196 1","pages":"110-4"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74494936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-01-01DOI: 10.1097/TA.0b013e31815eb776
J. Diaz, Patrick R. Norris, B. Collier, M. Berkes, A. Ozdas, A. May, Richard S. Miller, John A. Morris
BACKGROUND Age, Injury severity score (ISS), hyperglycemia (HGL) at admission, and morbid obesity are known risk factors of poor outcome in trauma patients. Our aim was to which risk factors had the highest risk of death in the critically ill trauma patient. METHODS A Trauma Registry of the American College of Surgeons database retrospective study was performed at our Level I trauma center from January 2000 to October 2004. Inclusion criteria were age >15 years and >or=3 days hospital stay. Data collected included age, gender, and ISS. Groups were divided into nonobese and morbidly obese (MO) (body mass index, BMI >or=40 kg/m2) and into HGL (mean >or=150 mg/dL on initial hospital day) and non-HGL. Primary outcome was 30-day mortality. Differences in mortality and demographic variables between groups were compared using Fisher's exact and Wilcoxon's rank sum tests. Univariate and multivariate logistic regression was used to assess the relationship of HGL, morbid obesity, age, and injury severity to risk of death. Relationships were assessed using odds ratios (OR) and area under the receiver operator characteristic curve (AUC). RESULTS A total of 1,334 patients met study criteria and 70.5% were male. Demographic means were age 40.3, ISS 25.7, length of stay 13.4, and BMI 27.5. The most common mechanism of injury was motor vehicle collision 55.1%. Overall mortality was 4.7%. Mortality was higher in HGL versus non-HGL (8.7% vs. 3.5%; p < 0.001). Mortality was higher in MO versus nonobese, but not significantly (7.8 vs. 4.6%; not significant [NS] p = 0.222). Univariate logistic regression relationships of death to age OR: 1.031, p < 0.001, AUC +/- SE: 0.639 +/- 0.042; ISS OR: 1.044, p < 0.001, AUC +/- SE: 0.649 +/- 0.039; HGL OR: 2.765, p < 0.001; MO: OR: NS, p = NS, AUC +/- SE: NS. Relationships were similar in a combined multivariate model. CONCLUSION HGL >150 mg/dL on the day of admission is associated with twofold increase in mortality, and an outcome measure should be followed. Morbid obesity (BMI >or=40) is not an independent risk factor for mortality in the critically ill trauma patient.
背景:年龄、入院时损伤严重程度评分(ISS)、高血糖(HGL)和病态肥胖是已知的创伤患者预后不良的危险因素。我们的目的是找出哪些危险因素对重症创伤患者的死亡风险最高。方法对2000年1月至2004年10月在我院一级创伤中心进行美国外科学会创伤登记数据库的回顾性研究。纳入标准为年龄>15岁且住院时间>或=3天。收集的数据包括年龄、性别和ISS。各组分为非肥胖和病态肥胖(MO)组(体重指数，BMI >或=40 kg/m2)， HGL组(入院首日平均>或=150 mg/dL)和非HGL组。主要终点为30天死亡率。使用Fisher精确检验和Wilcoxon秩和检验比较组间死亡率和人口统计学变量的差异。采用单因素和多因素logistic回归评估HGL、病态肥胖、年龄和损伤严重程度与死亡风险的关系。使用比值比(OR)和接受者操作者特征曲线下面积(AUC)评估两者之间的关系。结果共1334例患者符合研究标准，其中70.5%为男性。人口统计学平均值为年龄40.3,ISS 25.7，住院时间13.4,BMI 27.5。最常见的伤害机制是机动车碰撞，占55.1%。总死亡率为4.7%。HGL患者的死亡率高于非HGL患者(8.7% vs. 3.5%;P < 0.001)。非肥胖患者的死亡率比非肥胖患者高，但不显著(7.8比4.6%;无统计学意义[NS] p = 0.222)。死亡与年龄的单因素logistic回归关系OR: 1.031, p < 0.001, AUC +/- SE: 0.639 +/- 0.042;ISS OR: 1.044, p < 0.001, AUC +/- SE: 0.649 +/- 0.039;HGL OR: 2.765, p < 0.001;MO: OR: NS, p = NS, AUC +/- SE: NS。在一个组合的多变量模型中，关系是相似的。结论入院当日hgl >150 mg/dL与死亡率增加2倍相关，应采取结局措施。病态肥胖(BMI > =40)不是创伤危重症患者死亡的独立危险因素。
{"title":"Morbid obesity is not a risk factor for mortality in critically ill trauma patients.","authors":"J. Diaz, Patrick R. Norris, B. Collier, M. Berkes, A. Ozdas, A. May, Richard S. Miller, John A. Morris","doi":"10.1097/TA.0b013e31815eb776","DOIUrl":"https://doi.org/10.1097/TA.0b013e31815eb776","url":null,"abstract":"BACKGROUND Age, Injury severity score (ISS), hyperglycemia (HGL) at admission, and morbid obesity are known risk factors of poor outcome in trauma patients. Our aim was to which risk factors had the highest risk of death in the critically ill trauma patient. METHODS A Trauma Registry of the American College of Surgeons database retrospective study was performed at our Level I trauma center from January 2000 to October 2004. Inclusion criteria were age >15 years and >or=3 days hospital stay. Data collected included age, gender, and ISS. Groups were divided into nonobese and morbidly obese (MO) (body mass index, BMI >or=40 kg/m2) and into HGL (mean >or=150 mg/dL on initial hospital day) and non-HGL. Primary outcome was 30-day mortality. Differences in mortality and demographic variables between groups were compared using Fisher's exact and Wilcoxon's rank sum tests. Univariate and multivariate logistic regression was used to assess the relationship of HGL, morbid obesity, age, and injury severity to risk of death. Relationships were assessed using odds ratios (OR) and area under the receiver operator characteristic curve (AUC). RESULTS A total of 1,334 patients met study criteria and 70.5% were male. Demographic means were age 40.3, ISS 25.7, length of stay 13.4, and BMI 27.5. The most common mechanism of injury was motor vehicle collision 55.1%. Overall mortality was 4.7%. Mortality was higher in HGL versus non-HGL (8.7% vs. 3.5%; p < 0.001). Mortality was higher in MO versus nonobese, but not significantly (7.8 vs. 4.6%; not significant [NS] p = 0.222). Univariate logistic regression relationships of death to age OR: 1.031, p < 0.001, AUC +/- SE: 0.639 +/- 0.042; ISS OR: 1.044, p < 0.001, AUC +/- SE: 0.649 +/- 0.039; HGL OR: 2.765, p < 0.001; MO: OR: NS, p = NS, AUC +/- SE: NS. Relationships were similar in a combined multivariate model. CONCLUSION HGL >150 mg/dL on the day of admission is associated with twofold increase in mortality, and an outcome measure should be followed. Morbid obesity (BMI >or=40) is not an independent risk factor for mortality in the critically ill trauma patient.","PeriodicalId":92962,"journal":{"name":"The journal of cardiothoracic trauma","volume":"42 1","pages":"226-31"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74495882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-01-01DOI: 10.1097/TA.0b013e3181953bc4
T. Fabian
{"title":"The American Association for the Surgery of Trauma--through the looking glass: déjà vu all over again.","authors":"T. Fabian","doi":"10.1097/TA.0b013e3181953bc4","DOIUrl":"https://doi.org/10.1097/TA.0b013e3181953bc4","url":null,"abstract":"","PeriodicalId":92962,"journal":{"name":"The journal of cardiothoracic trauma","volume":"26 1","pages":"1-16"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83984507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-01-01DOI: 10.1097/TA.0b013e31815644e5
L. Saunders, Anbesaw Selassie, E. Hill, J. Nicholas, A. Varma, D. Lackland, Sunil J. Patel
BACKGROUND We aim to assess the long-term trend of and identify risk factors for traumatic spinal cord injury (TSCI) mortality from 1981 through 1998 in the state of South Carolina (SC). METHODS We analyzed data from the TSCI surveillance system in SC. Poisson regression analyses were used to examine trends in TSCI mortality rates across subpopulations of interest. Multiple logistic regression was used to identify risk factors for TSCI mortality. RESULTS The rate of TSCI mortality was 27.4 per million population between 1981 and 1998. A significant 3% annual decrease in the TSCI mortality rate was found from 1981 through 1998. Specifically, TSCI mortality rates declined the most per year in motor vehicle crashes, males, and whites. Adjusted for covariates, individuals of older ages, black race, with a cervical TSCI, and with a more severe injury, as defined by both Frankel grade and Abbreviated Injury Scale, were associated with higher odds of in-hospital mortality. Females had lower odds of in-hospital mortality than males. CONCLUSION Although mortality rate is decreasing, TSCI remains a significant public health problem, with SC having higher rates of TSCI mortality than the United States. The association between gender and in-hospital mortality needs further exploration.
{"title":"Traumatic spinal cord injury mortality, 1981-1998.","authors":"L. Saunders, Anbesaw Selassie, E. Hill, J. Nicholas, A. Varma, D. Lackland, Sunil J. Patel","doi":"10.1097/TA.0b013e31815644e5","DOIUrl":"https://doi.org/10.1097/TA.0b013e31815644e5","url":null,"abstract":"BACKGROUND We aim to assess the long-term trend of and identify risk factors for traumatic spinal cord injury (TSCI) mortality from 1981 through 1998 in the state of South Carolina (SC). METHODS We analyzed data from the TSCI surveillance system in SC. Poisson regression analyses were used to examine trends in TSCI mortality rates across subpopulations of interest. Multiple logistic regression was used to identify risk factors for TSCI mortality. RESULTS The rate of TSCI mortality was 27.4 per million population between 1981 and 1998. A significant 3% annual decrease in the TSCI mortality rate was found from 1981 through 1998. Specifically, TSCI mortality rates declined the most per year in motor vehicle crashes, males, and whites. Adjusted for covariates, individuals of older ages, black race, with a cervical TSCI, and with a more severe injury, as defined by both Frankel grade and Abbreviated Injury Scale, were associated with higher odds of in-hospital mortality. Females had lower odds of in-hospital mortality than males. CONCLUSION Although mortality rate is decreasing, TSCI remains a significant public health problem, with SC having higher rates of TSCI mortality than the United States. The association between gender and in-hospital mortality needs further exploration.","PeriodicalId":92962,"journal":{"name":"The journal of cardiothoracic trauma","volume":"2 1","pages":"184-90"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84213750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-01-01DOI: 10.1097/TA.0b013e31818b146d
Gregory W. Thomas, L. Rael, R. Bar-Or, R. Shimonkevitz, C. Mains, D. Slone, M. Craun, D. Bar-Or
BACKGROUND The cytotoxic effects of antiseptics on pivotal cell types of the healing process have been well documented. The purpose of our investigation was to explore the ability of subcytotoxic levels of antiseptics to interfere with fibroblast function. METHODS Cell proliferation assays were performed by culturing fibroblasts in the presence of commonly used antiseptics. Migration was evaluated using scratch assays in which monolayers were "wounded" and cellular movement was monitored by digital photography. Matrix metalloproteinase (MMP) release was analyzed by zymography. RESULTS H2O2 and povidone-iodine reduced both migration and proliferation of fibroblasts in a dose-dependent fashion. Treatment with silver-containing antiseptics and chlorhexidine exhibited reductions in proliferation at high concentrations, but enhanced growth at lower doses. Silver-containing compounds and chlorhexidine also proved to be the least detrimental to migration in these assays. metalloproteinase release from the cells was differently affected depending on the dosage and class of antiseptic applied. CONCLUSIONS When debridement of the wound bed is not sufficient to reduce bacterial loads, the application of broad-spectrum antiseptics maybe indicated. Our data would suggest that H2O2 and iodine are poor choices, potentially retarding the contribution of fibroblasts to the healing process. Silver sulfadiazine and chlorhexidine, at levels still proven to be bactericidal, had fewer detrimental effects on fibroblast activity in these assays. The silver-containing antiseptics may even increase the proliferative potential of these cells in culture.
{"title":"Mechanisms of delayed wound healing by commonly used antiseptics.","authors":"Gregory W. Thomas, L. Rael, R. Bar-Or, R. Shimonkevitz, C. Mains, D. Slone, M. Craun, D. Bar-Or","doi":"10.1097/TA.0b013e31818b146d","DOIUrl":"https://doi.org/10.1097/TA.0b013e31818b146d","url":null,"abstract":"BACKGROUND The cytotoxic effects of antiseptics on pivotal cell types of the healing process have been well documented. The purpose of our investigation was to explore the ability of subcytotoxic levels of antiseptics to interfere with fibroblast function. METHODS Cell proliferation assays were performed by culturing fibroblasts in the presence of commonly used antiseptics. Migration was evaluated using scratch assays in which monolayers were \"wounded\" and cellular movement was monitored by digital photography. Matrix metalloproteinase (MMP) release was analyzed by zymography. RESULTS H2O2 and povidone-iodine reduced both migration and proliferation of fibroblasts in a dose-dependent fashion. Treatment with silver-containing antiseptics and chlorhexidine exhibited reductions in proliferation at high concentrations, but enhanced growth at lower doses. Silver-containing compounds and chlorhexidine also proved to be the least detrimental to migration in these assays. metalloproteinase release from the cells was differently affected depending on the dosage and class of antiseptic applied. CONCLUSIONS When debridement of the wound bed is not sufficient to reduce bacterial loads, the application of broad-spectrum antiseptics maybe indicated. Our data would suggest that H2O2 and iodine are poor choices, potentially retarding the contribution of fibroblasts to the healing process. Silver sulfadiazine and chlorhexidine, at levels still proven to be bactericidal, had fewer detrimental effects on fibroblast activity in these assays. The silver-containing antiseptics may even increase the proliferative potential of these cells in culture.","PeriodicalId":92962,"journal":{"name":"The journal of cardiothoracic trauma","volume":"359 1","pages":"82-90; discussion 90-1"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77840334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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