ISSN:0022-5282    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:0022-5282    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Objective:To investigate the hypothesis that occult hypoperfusion (OH) is associated with infectious episodes in major trauma patients.Methods:Data were collected prospectively on all adult trauma patients admitted to the Surgical/Trauma Intensive Care Unit from November of 1996 to December of 1998. Treatment was managed by a single physician according to a defined resuscitation protocol directed at correcting OH (lactic acid [LA] > 2.4 mmol/L).Results:Of a total of 381 consecutive patients, 118 never developed OH and 263 patients exhibited OH. Seventeen patients were excluded because their LA never corrected, and they all subsequently died. One hundred seventy-six infectious episodes occurred in 97 of the 364 patients remaining. The infection rate in patients with no elevation of LA was 13.6% (n = 118) compared with 12.7% (n = 110) in patients whose LA corrected by 12 hours, 40.5% (n = 79;p< 0.01 compared with all other groups) in patients whose LA corrected between 12 and 24 hours, and 65.9% (n = 57;p< 0.01 compared with all other groups) in patients who corrected after 24 hours. Among the patients with infections, there were 276 infection sites with 42% of infections involving the lung and 21% involving bacteremia. There was no difference in proportion of infections occurring at each site between groups. The mortality rate of patients who developed infections was 7.9% versus 1.9% in patients without infections (p< 0.05). Of the patients who developed infections, 69.8% versus 25.8% (p< 0.001) did not have their lactate levels normalized within12 hours of emergency room admission. Logistic regression demonstrated that both the Injury Severity Score and OH > 12 hours were independently predictive of infection.Conclusion:A clear increase in infections occurred in patients with OH whose lactate levels did not correct by 12 hours, with an associated increase in length of stay, days in surgical/trauma intensive care unit, hospital charges, and mortality.

ISSN:0022-5282    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Objectives:New York State Trauma Registry data were analyzed to determine whether there is a significant relationship between the volume of trauma patients treated by a trauma center and its risk-adjusted inpatient mortality rate.Methods:Stepwise logistic regression was used to identify significant independent predictors of mortality, their weights, and the probability of in-hospital mortality for each patient. These data were then used to calculate risk-adjusted mortality rates for various ranges of hospital volume. Ranges were identified on the basis of homogeneity of mortality rates, the number of hospitals in each range, and the number of patients in each range. Three volume measures were used: (1) total annual volume of trauma cases ≥ 1200 and total annual volume ≥ 240 for patients with Injury Severity Score (ISS) ≥ 15 (equivalent to American College of Surgeons [ACS] criteria), (2) total annual volume of patients with ISS ≥ 15, and (3) total annual volume of cases in the Registry (approximately, inpatients with ISS ≥ 9).Results:Results show that the 35 New York State trauma centers not meeting the ACS criteria had lower, but not significantly lower, observed and risk-adjusted mortality rates (7.62% and 8.25%, respectively) than the corresponding rates for the 8 New York State trauma centers that met the ACS criteria (9.36% and 8.83%, respectively). Regarding the other two criteria, hospital ranges representing lower annual volumes tended to have somewhat lower, although not significantly lower, observed and risk-adjusted mortality rates. For example, using a total annual volume for patients with ISS ≥ 15, the risk-adjusted mortality rates for the volume ranges 1–150, 151–250, and 251+ were 7.78%, 9.23%, and 8.70%, respectively.Conclusions:We were unable to document an inverse relationship between hospital volume and inpatient mortality rate for trauma centers in New York State. Volume criteria should not be considered indicators of the quality of trauma care.

ISSN:0022-5282    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Background:Regional trauma systems were proposed 2 decades ago to reduce injury mortality rates. Because of the difficulties in evaluating their effectiveness and the methodologic limitations of previously published studies, the relative benefits of establishing an organized system of trauma care remains controversial.Methods:Data on trauma systems were obtained from a survey of state emergency medical service directors, review of state statutes and a previously published trauma system inventory. Injury mortality rates were obtained from national vital statistics data, whereas motor vehicle crash (MVC) mortality rates were obtained from the Fatality Analysis Reporting System. Mortality rates were compared between states with and without trauma systems.Results:As of 1995, 22 states had regional trauma systems. States with trauma systems had a 9% lower crude injury mortality rate than those without. When MVC-related mortality was evaluated separately, there was a 17% reduction in deaths. After controlling for age, state speed laws, restraint laws, and population distribution, there remained a 9% reduction in MVC-related mortality rate in states with a trauma system.Conclusion:These data demonstrate that a state trauma system is associated with a reduction in the risk of death caused by injury. The effect is most evident on analysis of MVC deaths.

ISSN:0022-5282    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Background:Lower torso ischemia and reperfusion leads to remote organ leukosequestration and injury. We now examine the intermediary role of selectins and complement in mediating lung and liver injury after hindlimb ischemia.Methods:Mice underwent a 2-hour bilateral tourniquet hindlimb ischemia followed by 3 hours of reperfusion.Results:Neutrophil depletion significantly decreased lung vascular permeability index (PI), measured by the extravasation of125I-albumin, and liver injury as assessed by serum alanine aminotransferse levels. Lung PI and serum alanine aminotransferse levels were also reduced in mice treated with recombinant soluble P-selectin glycoprotein ligand-immunoglobulin fusion protein. Complement inhibition with soluble complement receptor type 1 decreased lung PI and serum alanine aminotransferse levels. C5-deficient mice exhibited a similar decrease in lung PI and liver injury. Lung and liver injury were restored in C5-deficient mice reconstituted with wild-type serum.Conclusion:Remote organ injury after lower torso reperfusion is selectin and complement dependent.

ISSN:0022-5282    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Background:The liver plays a critical regulatory role in the acute inflammatory response to injury, although the mechanisms of this regulation are not well understood. transforming growth factor-&bgr;1(TGF-&bgr;1) is induced after burn injury and may contribute to an inhibitory or fatal effect on hepatocytes. We investigated the association over time between plasma concentration of TGF-&bgr;1, expression of TGF-&bgr;1m-RNA in liver tissue, and histologic analysis of liver apoptosis after burn injury.Methods:Male BALB/c mice were anesthetized and randomized to receive 0% (sham), moderate (approximately 25%) (M), or large (approximately 50%) (L) body surface area full-thickness contact burn, followed by resuscitation and analgesia. Animals were killed over a time course from 15 minutes to 24 hours after burn injury, and liver tissue and peripheral blood were collected. Plasma levels of TGF-&bgr;1(nanograms per milliliter) were measured by enzyme-linked immunosorbent assay. TGF-&bgr;1m-RNA was extracted from liver and measured by reverse transcription-polymerase chain reaction. Histology of liver apoptosis was examined after fixation and staining with TdT-mediated dUTP nick-end labeling (TUNEL) method.Results:The plasma concentration of TGF-&bgr;1in burn group L was significantly increased at 4 hours after burn when compared with sham and M burn groups. This rise in plasma TGF-&bgr;1was preceded by an increase in hepatic TGF-&bgr;1m-RNA expression at 30 minutes, 1, 2, and 4 hours after burn in the L group. Histologic analysis found greater hepatocyte death in the L group than in the M group at 8 hours after burn.Conclusion:The levels of induced TGF-&bgr;1and TGF-&bgr;1m-RNA after L burn injury are higher and peak earlier than after M burn injury. Elevated TGF-&bgr;1may be associated with cell death in hepatocytes. The TGF-&bgr;1rise may be associated with hepatocyte injury and systemic response to massive burn.

ISSN:0022-5282    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Objective:Neutrophil (PMN) priming after hemorrhagic shock is predictive of the subsequent development of multiple organ failure, but the mechanism remains unknown. Recently, we and others have demonstrated that mesenteric lymph from shock animals resuscitated with lactated Ringer’s solution (LR) is not only a potent PMN priming agent but also causes lung injury. Work by others has shown that resuscitation with hypertonic saline (HTS) protects animals from lung injury after hemorrhagic shock. Therefore, we hypothesize that resuscitation with HTS will abolish PMN priming by postshock mesenteric lymph.Methods:After mesenteric lymph duct catheterization, male rats underwent hemorrhagic shock (mean arterial pressure of 40 mm Hg for 90 minutes) and resuscitation with shed blood plus either LR (2× volume of shed blood) or 4 mL/kg of 7% HTS (isonatremic). Priming for superoxide by PMN was measured after fMLP (1 &mgr;M) activation.Results:Shock significantly decreased mesenteric lymph flow from preshock levels in both groups. LR resuscitation produced significantly more mesenteric lymph than HTS resuscitation. Mesenteric lymph from LR animals primed PMN for superoxide production, whereas, HTS eliminated this priming.Conclusion:HTS not only decreases postshock mesenteric lymph production, it eliminates PMN priming by mesenteric lymph, suggesting a mechanism for the beneficial effects of HTS resuscitation.

ISSN:0022-5282    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Objective:To investigate the effect of age on the metabolic response to injury.Methods:Fifty-two trauma patients meeting entrance criteria were prospectively enrolled. Patients were grouped by age: elderly, >60 years; and young, ≤60 years. After 4 days of nutrition support, physiologic and laboratory data were collected. Energy and nitrogen metabolism, and body composition were evaluated.Results:Elderly patients demonstrated a reduced incidence of fever (48% vs. 77%,p= 0.027). Independent of body composition, temperature, and injury severity, oxygen consumption was 8% lower in the elderly (p= 0.0032). However, nitrogen loss and myofibrillar catabolic rate was not altered by age. Elderly subjects were more often hyperglycemic (38% vs. 0%,p< 0.0001) and azotemic (62% vs. 22%,p= 0.004), despite similar carbohydrate and protein intake.Conclusion:Fever is less common and oxygen consumption lower in elderly trauma patients. Postinjury myofibrillar protein catabolism and nitrogen loss are not influenced by aging. Metabolic complications of nutrition support (hyperglycemia, azotemia) are more common in elderly trauma patients.

ISSN:0022-5282    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Background:Although hypothermia often occurs after trauma and has protective effects during ischemia and organ preservation, it remains unknown whether maintenance of hypothermia or restoring the body temperature to normothermia during resuscitation has any deleterious or beneficial effects on heart performance and organ blood flow after trauma-hemorrhage.Methods:Male rats underwent laparotomy (i.e., induced trauma) and were exsanguinated to and maintained at a mean arterial pressure of 40 mm Hg until 40% of the maximum shed volume was returned in the form of Ringer’s lactate. Body temperature decreased from approximately 36.5°C to below 32°C. The animals were then resuscitated with four times the volume of maximal bleedout with Ringer’s lactate. In one group, body temperature was rewarmed to 37°C during resuscitation. In another group, body temperature was maintained at hypothermia (32°C) for 4 hours after resuscitation. In an additional group, the body temperature was kept at 37°C during hemorrhage as well as during resuscitation. Left ventricle performance parameters such as maximal rate of left ventricular pressure increase and decrease (±dP/dtmax) were measured up to 4 hours. Cardiac output and regional blood flow were determined by radioactive microspheres at 4 hours after the completion of resuscitation.Results:The maintenance of normothermia during hemorrhage or prolonged hypothermia after resuscitation depressed the left ventricular performance parameters, cardiac output, and regional blood flow in various organs. Rewarming the body to normothermia during resuscitation, however, significantly increased heart performance, cardiac output (from hypothermia 16.2 ± 1.4 to 22.3 ± 1.4 mL/min per 100 g body weight,p< 0.05) and total hepatic blood flow (from hypothermia 117.5 ± 5.3 to 166.0 ± 9.3 mL/min per 100 g tissue,p< .05).Conclusion:Our data indicate that restoration of normothermia during resuscitation improves cardiac function and hepatic blood flow compared with hypothermia.

ISSN:0022-5282    

出版商:OVID    

年代:2000

数据来源: OVID