Biomedical subjects

Saman Arbabi

Publications and source records attributed to Saman Arbabi.

At least 19 recordsLinked to original sources

PubMed2007

Beta-blocker use is associated with improved outcomes in adult trauma patients.

BACKGROUND: Beta-adrenoreceptor blocker (beta-blocker) therapy may improve outcomes in surgical patients by decreasing cardiac oxygen consumption and hypermetabolism. Because beta-blockers can lower the systemic blood pressure and cerebral perfusion pressure, there is concern regarding their use in patients with head injury. However, beta-blockers may protect beta-receptor rich brain cells by attenuating cerebral oxygen consumption and metabolism. We hypothesized that beta-blockers are safe in trauma patients, even if they have suffered a significant head injury. METHODS: Using pharmacy and trauma registry data of a Level I trauma center, we identified a cohort of trauma patients who received beta-blockers during their hospital stay (beta-cohort). Trauma admissions who did not receive beta-blockers were in the control cohort. beta-blocker status, in combination with other variables associated with mortality, were placed in a stepwise multivariate logistic regression to identify independent predictors of fatal outcome. RESULTS: In all, 303 (7%) of 4,117 trauma patients received beta-blockers. In the beta-cohort, 45% of patients were on beta-blockers preinjury. The most common reason to initiate beta-blocker therapy was blood pressure (60%) and heart rate (20%) control. The overall mortality rate was 5.6% and head injury was considered to be the major cause of death. After adjusting for age, Injury Severity Scale score, blood pressure, Glasgow Coma Scale score, respiratory status, and mechanism of injury, the odds ratio for fatal outcome was 0.3 (p < 0.001) for beta-cohort as compared with control. Decreased risk of fatal outcome was more pronounced in patients with a significant head injury. CONCLUSIONS: beta-blocker therapy is safe and may be beneficial in selected trauma patients with or without head injury. Further studies looking at beta-blocker therapy in trauma patients and their effect on cerebral metabolism are warranted.

Adrenergic beta-Antagonists↗

PubMed2006

Attenuating burn wound inflammatory signaling reduces systemic inflammation and acute lung injury.

The relationship between local inflammation and the subsequent systemic inflammatory response is poorly described. In a burn injury model, the dermal inflammatory response may act as an ongoing trigger for the systemic inflammatory response syndrome (SIRS) and subsequent systemic complications. We hypothesized that topical attenuation of burn wound inflammatory signaling will control the dermal inflammatory source, attenuate SIRS, and reduce acute lung injury. Mice received a 30% total body surface area burn. Subgroups were treated with specific p38 MAPK inhibitor or vehicle, which was topically applied to wounds. Topical p38 MAPK inhibition significantly reduced burn wound inflammatory signaling and subsequent systemic expression of proinflammatory cytokines and chemokines. In vitro macrophage functional assays demonstrated a significant attenuation in serum inflammatory mediators from animals receiving the topical inhibitor. Topical p38 MAPK inhibition resulted in significantly less pulmonary inflammatory response via reduction of pulmonary neutrophil sequestration, pulmonary cytokine expression, and a significant reduction in pulmonary microvascular injury and edema formation. Although dermal activating transcription factor-2, a downstream p38 MAPK target, was significantly reduced, there was no reduction in pulmonary activating transcription factor-2 expression, arguing against significant systemic absorption of the topical inhibitor. These experiments demonstrate a strong interaction between dermal inflammation and systemic inflammatory response. Attenuating local inflammatory signaling appears effective in reducing SIRS and subsequent systemic complications after burn injury.

Animals↗

PubMed2006

Use of computerized ICU documentation to capture ICU core measures.

BACKGROUND: Intensive care unit (ICU) core measures that target the prevention of catheter-related bloodstream infections (CRBSIs) and ventilator-associated pneumonia (VAP) in ventilated ICU patients are underway across the United States. Implementation often requires additional personnel to educate providers and collect the data. We hypothesized that use of our current computerized ICU flowsheet could provide timely, accurate data on ICU core measures without additional personnel dedicated to data capture. METHODS: In a 10-bed, closed surgical ICU with existing protocols for deep vein thrombosis (DVT) prophylaxis, stress ulcer bleeding prophylaxis (SUP), ventilator weaning parameters, and glucose control, we created a reporting tool that would document daily weaning parameters, head of bed (HOB) at 30 degrees , glucose levels, DVT prophylaxis, and SUP. Our glucose protocol targeted <150 mg/dL, with all daily glucose values reported rather than just the morning value. The results from the previous 12 am to 11:59 pm were available to the rounding team at 7 am. We examined compliance at the start and after education of medical staff (March/April for HOB up, DVT, and SUP; May/June for glucose control). RESULTS: During 2005, compliance with all protocols improved. Percent compliance for DVT prophylaxis, SUP, and HOB up rose from as low as 32% at the start of the documentation process to consistently higher than the target level of 95%. Compliance for glucose control increased after intensive education of nursing and physicians with the mean glucose falling from 144 to 122 mg/dL. There was increased nursing workload for checking glucose levels in which the mean number of glucose checks rose from a low of 1.5 per patient to as high as 8.2 per patient per day. CRBSI and VAP rates did not decrease during this period compared with the prior year. Length of stay and mortality were unchanged. CONCLUSIONS: Reporting of ICU core measures to treating staff can be done accurately and promptly with a computerized system. Education was effective in improving compliance levels. No additional personnel were required to create reports, capture data, or improve compliance after initial development and testing. Although compliance with core measures met target levels at the end of the year, we did not observe improved outcomes in terms of CRBSI, VAP, mortality, or length of stay.

APACHE↗

PubMed2006

Advances in burn critical care.

BACKGROUND: Management of burn patients requires a complex interaction of surgical, medical, critical care, and rehabilitation approaches. Severe burn patients are some of the most challenging critically ill patients who may have multiple-system organ failure with life-threatening complications. OBJECTIVE: To review and highlight some of the recent advances in burn critical care. We focused on some of the new treatment modalities in the management of respiratory complications, advances in burn resuscitation, management of the metabolic response to burns, and recent ideas in burn immunotherapy. DATA SOURCE: A search of the MEDLINE database and manual review of published articles and abstracts from national and international meetings. DATA SYNTHESES AND CONCLUSIONS: The respiratory management of burn patients includes strategies to minimize iatrogenic injury with low tidal volume ventilation, to improve ventilation/perfusion mismatch, and to diagnosis pneumonia. Many aspects of burn resuscitation remain controversial, and the best form of fluid resuscitation has yet to be identified. Recent research in the metabolic response to thermal injury has identified many potentially beneficial treatments. Although immunomodulation therapy is promising, currently most of these treatments are not clinically viable, and further clinical and translational research is warranted.

Adrenergic beta-Antagonists↗

PubMed2006

Cardiomyocyte function after burn injury and lipopolysaccharide exposure: single-cell contraction analysis and cytokine secretion profile.

A component of multiorgan dysfunction in burned patients is heart failure. Burn trauma induces cytokine synthesis of interleukin (IL) 1beta, IL-6, and tumor necrosis factor alpha (TNF-alpha) which can negatively impact cardiac function. Infectious complications are common following severe burn injury. We hypothesized that burn injury and lipopolysaccharide (LPS) exposure independently influence peak cardiomyocyte contraction and cytokine secretion. Rats underwent a full-thickness 30% total body surface area scald or sham burn. At 1, 6, 12, and 24 h after burn, cardiomyocytes were isolated and incubated with increasing LPS doses. Peak sarcomere shortening and contractile velocity parameters were recorded using a variable-rate video camera with sarcomere length detection software. Supernatants were assayed for IL-1beta, IL-6, and TNF-alpha by ELISA. Peak sarcomere shortening was decreased in the burn group at 1, 6, 12, and 24 h after burn. IL-1beta, IL-6, and TNF-alpha levels were increased in cardiomyocytes isolated 1 h after burn compared with sham controls, but returned to sham levels at 6, 12, and 24 h after burn. LPS exposure caused dose-dependent decreases in sarcomere shortening in sham and burn animals. LPS exposure did not produce increased cardiomyocyte cytokine expression. Burn injury diminished peak sarcomere shortening. Whereas exposure to LPS did not have an effect on cardiomyocyte cytokine expression, LPS significantly inhibited sarcomere shortening in a dose-dependent fashion. Combined burn and LPS exposure inhibited sarcomere shortening more than each alone. These results demonstrate that LPS exposure and burn injury independently decrease peak cardiac shortening. These decreases did not directly correlate with the levels of cytokines released in response to each stressor.

Animals↗

PubMed2006

Topical p38MAPK inhibition reduces dermal inflammation and epithelial apoptosis in burn wounds.

Thermal injury induces dermal inflammatory and proapoptotic signaling. These phenomena extend burn wound size and trigger a systemic inflammatory response, factors known to adversely affect outcomes. p38MAPK is known to trigger inflammatory responses and induce epithelial proapoptotic genes. We hypothesize that topical p38MAPK inhibition will attenuate excessive inflammatory and apoptotic signaling and reduce dermal tissue loss. Rats were given a 30% total body surface area partial thickness burn or sham injury. Some of the animals were treated with a p38MAPK inhibitor or vehicle, which was applied directly to the wound. Dermal inflammation was investigated with enzyme-linked immunosorbent assay, reverse transcriptase polymerase chain reaction, myeloperoxidase assay, and Evans blue extravasation. Apoptotic changes were detected using terminal deoxynucleotidyl transferase dUTP nick-end labeling assay and Caspase-3 in situ staining. Burn injury activated dermal p38MAPK and induced a significant rise in dermal IL-6, TNF-alpha, and IL-1beta expression. Neutrophil sequestration, microvascular damage, and hair follicle apoptosis were significantly elevated after injury. Topical p38MAPK inhibition significantly attenuated downstream dermal p38MAPK targets, proinflammatory cytokine expression, neutrophil sequestration, and microvascular injury. A significant reduction in hair follicle apoptosis was seen. This study demonstrates the attenuation of burn-induced cellular stress by topical application of p38MAPK inhibitors. Blunting early excessive inflammatory signaling may be an efficient strategy to improve patient outcomes after burn injury.

Administration, Topical↗

PubMed2006

Gene therapy with lipopolysaccharide binding protein for gram-negative pneumonia: respiratory physiology.

BACKGROUND: Lipopolysaccharide binding protein (LBP) plays an essential role in the pulmonary immune response to gram-negative bacterial infection. LBP knockout mice with gram-negative pneumonia have increased mortality compared with wild-type controls. This mortality difference can be abolished with systemic LBP gene therapy. We postulate that LBP knockout mice will develop derangements in lung physiology from gram-negative pneumonia and that these changes can be reversed with systemic LBP gene therapy. METHODS: Twelve- to 16-week-old C57BL/6 wild-type mice and/or sex, age, matched LBP knockout mice were administered 1 x 10(3) colony-forming units/mouse of Klebsiella pneumoniae by intratracheal inoculation. Treated mice were administered 5 x 10(9) plaque-forming units of recombinant adenovirus containing either the gene for LBP or the irrelevant control protein beta-galactosidase by intravenous injection 2 days before bacterial inoculation. Respiratory physiology parameters were measured preinoculation and 24 hours postbacterial inoculation. RESULTS: Administration of LBP by systemic gene therapy to LBP knockout mice improved 7-day survival from Klebsiella pneumonia to a level equivalent to wild-type mice exposed to the same dose of bacteria (42 vs. 43% survival). LBP knockout mice given the LBP gene therapy demonstrated increased 14-day survival from Klebsiella pneumonia when compared with controls treated with beta-galactosidase (28 vs. 0%, p < 0.001). LBP knockout mice developed significant differences in respiratory rate, minute ventilation, and enhanced pause (Penh), when compared with wild-type mice with Klebsiella pneumonia. These respiratory derangements were prevented with adenoviral delivery of the LBP gene before K. pneumoniae inoculation. CONCLUSIONS: Gram-negative pneumonia produces measurable changes in mortality and respiratory physiology between wild-type and LBP knockout mice. These changes can be prevented in LBP knockout mice by systemic gene therapy to restore innate immunity.

Acute-Phase Proteins↗

PubMed2005

An essential role for complement C5a in the pathogenesis of septic cardiac dysfunction.

Defective cardiac function during sepsis has been referred to as "cardiomyopathy of sepsis." It is known that sepsis leads to intensive activation of the complement system. In the current study, cardiac function and cardiomyocyte contractility have been evaluated in rats after cecal ligation and puncture (CLP). Significant reductions in left ventricular pressures occurred in vivo and in cardiomyocyte contractility in vitro. These defects were prevented in CLP rats given blocking antibody to C5a. Both mRNA and protein for the C5a receptor (C5aR) were constitutively expressed on cardiomyocytes; both increased as a function of time after CLP. In vitro addition of recombinant rat C5a induced dramatic contractile dysfunction in both sham and CLP cardiomyocytes, but to a consistently greater degree in cells from CLP animals. These data suggest that CLP induces C5aR on cardiomyocytes and that in vivo generation of C5a causes C5a-C5aR interaction, causing dysfunction of cardiomyocytes, resulting in compromise of cardiac performance.

Animals↗

PubMed2005

Lipopolysaccharide-binding protein modulates acetaminophen-induced liver injury in mice.

Acetaminophen toxicity is the most common cause of acute liver failure in the United States and Europe. Although much is known about the metabolism of acetaminophen, many questions remain regarding the pathogenesis of liver injury. In this study, we examined the role of lipopolysaccharide-binding protein (LBP), a protein important in mediating cellular response to lipopolysaccharides, by using LBP wild-type and knockout (KO) mice. We found that LBP KO mice were protected from acetaminophen-induced hepatotoxicity. At 350 mg/kg of acetaminophen, LBP KO mice had significantly less liver injury and necrosis than wild-type mice. Repletion studies in LBP KO mice using an LBP-adenoviral construct resulted in significantly more hepatic injury and necrosis after acetaminophen exposure compared with mice receiving the control adenoviral construct. In conclusion, LBP KO mice are protected from toxicity with a decrease in hepatic necrosis following acetaminophen challenge. This suggests a novel role for LBP in modulating acetaminophen-induced liver injury. Supplementary material for this article can be found on the HEPATOLOGY website (http://interscience.wiley.com/jpages/O270-9139/suppmat/index.html).

Acetaminophen↗

PubMed2005

Altered Kupffer cell function in biliary obstruction.

BACKGROUND: An altered Kupffer cell (KC) response is thought to be responsible for the characteristic phenotype observed after biliary obstruction: a phenotype marked by a defect in the hepatic reticuloendothelial system and a hypersensitivity to endotoxin. Few studies, however, have directly examined KC function. We have sought to define the specific alterations in function and phenotype that occur in the KC after biliary obstruction. METHODS: KCs were isolated from female C57BL/6 mice 4 days after a sham or common bile duct ligation (CBDL) operation. Phagocytosis, oxidative burst potential, and intracellular bacterial killing were measured as markers of reticuloendothelial system function. The KC response to endotoxin was assessed by measuring tumor necrosis factor alpha and interleukin 6 levels in the media after stimulation with lipopolysaccharide (LPS) or with LPS plus LPS-binding protein (LBP). RESULTS: CBDL KCs demonstrated a significant increase in phagocytic ability and significantly decreased baseline oxidative stress, compared with Shams. The oxidative burst potential, however, was equivalent or higher for CBDL KCs. CBDL KCs also demonstrated increased numbers of viable intracellular bacteria after infection; however, it is unclear if this finding represents impaired intracellular bacterial killing or increased phagocytosis of bacteria. With respect to the KC response to endotoxin, CBDL KCs were found to be less sensitive to the stimulatory effects of LPS alone but were exquisitely sensitive to the effects of LBP. LBP levels were found to be significantly elevated in CBDL animals, and CBDL KCs demonstrated a dose-dependent, exaggerated tumor necrosis factor alpha and interleukin 6 response to LPS administered with LBP. CONCLUSIONS: KC function is clearly altered after biliary obstruction. Phagocytic ability is actually increased, although the ability of CBDL KCs to kill bacteria within the phagosome remains ill defined. CBDL KCs are exquisitely sensitive to the effects of LBP, and LBP levels are elevated after biliary obstruction. LBP may be responsible for the increased proinflammatory response observed after endotoxin challenge in animals with biliary obstruction.

Acute-Phase Proteins↗

PubMed2005

Diagnosis and management of bile leaks after blunt liver injury.

BACKGROUND: Nonoperative management (NOM) of blunt liver injuries (BLIs) is common, but little data exist on the management of complications related to NOM. Furthermore, bile leaks are emerging as frequent complications of NOM. The goal of this study was to determine which BLI patients are at greatest risk for bile leaks and how to manage this complication. METHODS: Patients treated with NOM, including angiographic embolization (AE) and observation, were compared with those undergoing operation (OR). Mortality, hospital length of stay, liver-related complications, and severity of liver injury were compared among the groups. RESULTS: Two hundred eighty-one patients sustained a BLI from 1997 through 2004. The Injury Severity Score and age of the groups were similar. The mortality rate of the OR patients was higher (P = .02). All bile leaks occurred in patients with a liver Abbreviated Injury Score (AIS) of > or = 4. For survivors of more than 4 days, 71% of OR, 50% of AE, and 17% of observed patients developed bile leaks. For the OR and AE groups, HIDA scanning detected all leaks, leading to earlier drainage procedures. Detection of a bile leak in NOM patients before 5 days of hospitalization led to shorter HLOS, P = .02. No patient with a negative HIDA scan developed a subsequent bile leak. CONCLUSIONS: NOM of BLIs is associated with lower mortality, but significant complications. Bile leaks are more common in patients with higher liver AIS, and in this study presented in only those with liver AIS > or = 4. HIDA scanning successfully diagnosed all patients with bile leaks and led to less invasive drainage procedures over time and shorter HLOS.

Adult↗

PubMed2005

Improved survival in mice given systemic gene therapy in a gram negative pneumonia model.

BACKGROUND: We previously demonstrated an essential role for lipopolysaccharide binding protein (LBP) in the pulmonary immune response to Gram-negative bacterial infection. LBP knockout mice had significantly higher mortality, greater rates of bacteremia, and higher counts of viable bacteria in their lungs at sacrifice compared with wild-type controls. We postulate that systemic LBP gene therapy will reconstitute a protective innate immune response in LBP knockout mice and that overexpression of LBP in wild-type mice may offer a survival advantage. METHODS: 12-16 week old female C57BL/6 wild-type mice and age matched LBP knockout mice were given 5 x 10(9) PFU of recombinant adenovirus containing either the gene for LBP or the irrelevant control protein beta-galactosidase by tail vein injection. 72 hours later each mouse was administered 1 x 10(3) CFU of Klebsiella pneumoniae by intratracheal injection. RESULTS: Administration of LBP by systemic gene therapy to LBP knockout mice improved survival from Klebsiella pneumonia to a level equivalent or better than wild-type mice exposed to the same dose of bacteria (36 versus 25%). Wild-type mice given the LBP gene therapy demonstrated increased 7 day survival from Klebsiella pneumonia when compared with controls treated with beta-galactosidase (68 versus 30%, p = 0.03). CONCLUSIONS: Systemic gene therapy with intravenous adenoviral vector transfer of LBP significantly improves survival in LBP knockout mice. Overexpression of LBP in wild-type mice improves survival from Klebsiella pneumonia. Raising levels of LBP in the setting of Gram-negative pneumonia may be of therapeutic benefit.

Acute-Phase Proteins↗

PubMed2005

Effect of patient load on trauma outcomes in a Level I trauma center.

OBJECTIVE: Increased medical staff workload has been associated with worse outcomes in several studies. Inappropriate staffing has also been implicated in the increased risk of mortality for medical patients admitted on weekends. A theoretical threshold patient load may exist, beyond which the resources are strained and patient outcomes suffer. The goal of the study was to see whether trauma patients admitted during 'high' patient-load periods, at night, or on weekends had worse outcomes. METHODS: Trauma patients admitted to a high-volume Level I trauma center from 1994 to 2002 were analyzed. Patient load was defined as a combination of the number of patients admitted and the severity of their illness. On the basis of a multivariate regression model, a probability of fatal outcome was calculated for each patient as a marker for the severity of illness. For each patient, two new variables were calculated, the number of admissions (#ad) and the average probability of fatal outcome (PFO) for the 24-hour period in which the patient was admitted (excluding the patient him- or herself). The above variables, night/d, and weekend/d were placed in a multivariate regression model. RESULTS: There were 30,686 patients. Age, mechanism of injury, Injury Severity Score, maximum head Abbreviated Injury Scale score, admission Glasgow Coma Scale score, systolic blood pressure, and intubation status were the independent predictors of mortality. This model had an outstanding predictive power, with an area under the receiver operating characteristic curve of 0.96. The mean #ad was 11 +/- 4 and PFO was 0.08 +/- 0.07. Values above the 90th percentile were considered 'high' for #ad > 17 or PFO > 0.18. There was no difference in mortality for patients admitted during high #ad (odds ratio [OR], 0.95; p = 0.7) or high PFO (OR, 0.99; p = 0.9) versus low. There was no difference in mortality if a patient was admitted on weekends versus weekdays (OR, 0.9; p = 0.2) or at night versus day (OR, 0.9; p = 0.2). There was no difference in hospital length of stay for high #ad, high PFO, nights, or weekends. CONCLUSION: At this Level I trauma center that is part of an established statewide trauma system, patient outcomes were not compromised during high-patient-load periods, at night, or on weekends.

Adult↗

PubMed2004

Blunt splenic injury: operation versus angiographic embolization.

BACKGROUND: Splenic injuries, like other blunt traumatic injuries, are increasingly treated with non-operative management. Angiographic embolization (AE) has emerged as an alternative modality for treatment of splenic injuries. We hypothesized that splenic embolization would lead to equivalent, if not improved, outcomes in terms of mortality, total costs, complications, and duration of stay. METHODS: A retrospective review of a prospective data set was performed for all adult splenic injuries admitted to our level I trauma center from 2000 through 2003. Demographics, number of red cell units, emergency department hemodynamics, costs, and outcomes were examined. The operative group included those who underwent computed tomography (CT) first then went to the operating room (OR) (CT+OR) or those who went directly to the OR. RESULTS: There were 25 CT+OR and 24 AE patients of 164 blunt splenic injuries. After univariate analysis, higher injury severity score (ISS), lower systolic blood pressure, lower pH, and higher packed red blood cell transfusions were associated with increased mortality and duration of stay. The splenic Abbreviated Injury Scale (AIS; mean +/- SD) was the same for AE compared to CT+OR patients (3.8 +/- 0.4 vs 3.5 +/- 0.9). Although the AE group was older (50 +/- 20 vs 36 +/- 13 years, P < .01), Glasgow Comma Score (13 +/- 4 vs 11 +/- 5), age, highest heart rate (109 +/- 24 vs 120 +/- 43), and splenic AIS were not predictive of the need for an operation. Abdominal complications were lower in the AE group compared to the CT+OR (13% vs 29%), but mortality was not different (8% vs 4%). Total costs were similar for both groups after adjustment for ISS, GCS, pH, pretreatment transfusions, and spleen AIS (AE, $49,300 +/- $40,460 vs CT+OR, $54,590 +/- $34,760). The non-operative failure rate in this study was 2%. CONCLUSIONS: AE of splenic injuries is safe and associated with fewer complications. The spleen AIS, heart rate, age, and GCS did not correlate with the need for an operation. Higher ISS, lower blood pressure, lower pH, and increased number of packed red blood cell transfusions were better indicators of the need for an operation versus embolization.

Adult↗

PubMed2004

Extracorporeal life support for severe acute respiratory distress syndrome in adults.

OBJECTIVE: Severe acute respiratory distress syndrome (ARDS) is associated with a high level of mortality. Extracorporeal life support (ECLS) during severe ARDS maintains oxygen and carbon dioxide gas exchange while providing an optimal environment for recovery of pulmonary function. Since 1989, we have used a protocol-driven algorithm for treatment of severe ARDS, which includes the use of ECLS when standard therapy fails. The objective of this study was to evaluate our experience with ECLS in adult patients with severe ARDS with respect to mortality and morbidity. METHODS: We reviewed our complete experience with ELCS in adults from January 1, 1989, through December 31, 2003. Severe ARDS was defined as acute onset pulmonary failure, with bilateral infiltrates on chest x-ray, and PaO2/fraction of inspired oxygen (FiO2) ratio < or =100 or A-aDO2 >600 mm Hg despite maximal ventilator settings. The indication for ECLS was acute severe ARDS unresponsive to optimal conventional treatment. The technique of ECLS included veno-venous or veno-arterial vascular access, lung "rest" at low FiO2 and inspiratory pressure, minimal anticoagulation, and optimization of systemic oxygen delivery. RESULTS: During the study period, ECLS was used for 405 adult patients age 17 or older. Of these 405 patients, 255 were placed on ECLS for severe ARDS refractory to all other treatment. Sixty-seven percent were weaned off ECLS, and 52% survived to hospital discharge. Multivariate logistic regression analysis identified the following pre-ELCS variables as significant independent predictors of survival: (1) age (P = 0.01); (2) gender (P = 0.048); (3) pH < or =7.10 (P = 0.01); (4) PaO2/FiO2 ratio (P = 0.03); and (5) days of mechanical ventilation (P < 0.001). None of the patients who survived required permanent mechanical ventilation or supplemental oxygen therapy. CONCLUSION: Extracorporeal life support for severe ARDS in adults is a successful therapeutic option in those patients who do not respond to conventional mechanical ventilator strategies.

Adolescent↗

PubMed2004

Delayed repair for blunt thoracic aortic injury: is it really equivalent to early repair?

BACKGROUND: Blunt thoracic aortic injury (BTAI) is a severe injury that traditionally has mandated immediate surgical repair. Delaying operative intervention for BTAI can allow other life-threatening injuries to be managed first, but potentially increases the risk of aortic rupture and death. The objective of this study was to evaluate the outcome of delayed repair (DR) compared with early repair (ER) for BTAI and to assess the effectiveness of a protocol for medical control of systolic blood pressure and heart rate in those patients whose repairs were delayed. METHODS: This study is a retrospective review of University of Michigan Health System (UMHS) data from January 1, 1992, through March 1, 2003. ER was defined as operative repair within 16 hours from the time of injury. A similar analysis was conducted for patients with BTAI selected from the National Trauma Data Bank. RESULTS: For the UMHS data, there were 45 patients in the DR group and 33 patients in the ER group. Mortality in the ER group versus the DR group was 9% versus 20%. Multivariate analysis adjusting for age, Injury Severity Score, abdominal Abbreviated Injury Scale score, Glasgow Coma Scale score, and intubation status demonstrated an odds ratio for death from ER compared with DR of 1.72 (p = 0.57). Patients undergoing DR had an absolute increase in hospital length of stay (33.1 vs. 20.9 days) and complication rate (2.1 vs. 1.5 incidents per patient). A similar result was obtained for multivariate analysis of the National Trauma Data Bank data, with an odds ratio of 1.40 (p = 0.51) for death from ER versus DR. UMHS patients whose repairs were delayed achieved target systolic blood pressure and heart rate for 76% and 74% of the hourly measurements recorded, respectively. CONCLUSION: Patients with BTAI can safely undergo delayed aortic repair if other injuries warrant a higher treatment priority without increasing their overall risk of mortality. Delayed repair is, however, associated with a higher complication rate.

Adult↗

PubMed2004

Beta-blocker use is associated with improved outcomes in adult burn patients.

BACKGROUND: There is no direct evidence that beta-blockers improve mortality in burn victims. Beta-blockers attenuate hypermetabolic states in burned children, and perioperative use in elective adult cases has beneficial effects, which suggests that beta-blockers may also improve burn outcomes. However, beta-blockers decrease cardiac output and may decrease oxygen delivery, and theoretically may increase mortality. What is the effect of beta-blockers on healing time and mortality in burn patients? METHODS: This was a retrospective cohort study. We identified three cohorts of adult burn patients between 1996 and 2001: all who were on beta-blockers (BB) before their injury (PMH BB); all who were initiated on BB during their hospitalization for management of hypertension or tachyarrhythmia (HOSP BB); and control, who were never treated with beta-blockers. For each patient in the PMH BB and HOSP BB groups, two patients were placed in the control cohort by matching age and total body surface area burn. Premorbid conditions such as diabetes, hypertension, cardiac disease, renal insufficiency, and diuretic and calcium channel blocker use were analyzed. Multivariate regression models were used to identify independent modifiers. RESULTS: There were 21 PMH BB, 22 HOSP BB, and 86 control patients. All PMH BB patients remained on their BB regimen in the hospital. HOSP BB patients were initiated on beta-blockers at a mean of 8.8 days postinjury. There were no differences in age (mean, 58 +/- 17 years), total body surface area burned (mean, 14 +/- 12%), or mechanism of injury among the cohorts. The mortality rate was 5% for the PMH BB cohort, 27% for the HOSP BB cohort, and 13% for controls. The mean healing times were 51 +/- 29 days for PMH BB patients, 79 +/- 54 days for HOSP BB patients, and 60 +/- 39 for controls. In multivariate analyses, PMH BB was associated with a significant decrease in fatal outcome and healing time (p < or = 0.05 compared with control). CONCLUSION: Beta-blockers have the potential to improve adult burn outcomes. Postinjury treatment should be studied in a randomized, clinical trial.

Adrenergic beta-Antagonists↗

PubMed2004

A comparison of prehospital and hospital data in trauma patients.

OBJECTIVE: The use of prehospital data as an indicator for trauma team activation has been established. The relationship between field (Fd) and emergency department (ED) systolic blood pressure (SBP), Glasgow Coma Scale (GCS) score, and airway control as it relates to outcomes is unclear. We hypothesized that ED and Fd physiologic parameters are equally valid predictors of outcomes. In addition, we hypothesized that early field intubation will improve survival compared with later ED intubation. METHODS: Trauma registry data from two academic Level I centers from 1994 to 2001, excluding all transfers and burn patients, were analyzed using Wilcoxon signed-rank test and multivariate logistic regression with appropriate adjustments. RESULTS: There were 19,409 patients, 16,277 blunt and 3,132 penetrating trauma. There were 3,571 Fd and 746 ED intubations. ED intubation was associated with increased risk of fatal outcome compared with nonintubated patient (adjusted odds ratio, 3.1; p < 0.0001) and field intubations (adjusted odds ratio, 3.0; p < 0.0001). ED-GCS score was not significantly different from Fd-GCS score, with 82% having the same GCS category. This was not the case for SBP, and only in 60% of the cases were ED-SBP and Fd-SBP in the same category. In 31% of the patients, the ED-SBP increased, and in 9% of cases, the ED-SBP decreased compared with Fd-SBP. This was true for both blunt and penetrating trauma. Both Fd-SBP and ED-SBP were independent predicators of fatal outcome, and mortality rate significantly increased if ED-SBP category decreased compared with Fd-SBP. CONCLUSION: Early field intubation was associated with a decreased risk of fatal outcome compared with ED intubation. ED-GCS score was not significantly different from Fd-GCS score, and either one can be used to predict fatal outcome. However, ED-SBP was different from Fd-SBP in 40% of the patients, with the majority of cases having higher ED-SBP. Although ED-SBP was a better predictor of outcome, the best model is achieved when both ED and field SBP are used.

Adult↗