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Moderate Injury (moderate + injury)
Selected AbstractsClinical study of cats injured and killed in road traffic accidents in CambridgeshireJOURNAL OF SMALL ANIMAL PRACTICE, Issue 8 2004I. Rochlitz Data were collected on the injuries, treatment and outcome of 128 cats involved in road accidents and seen as first-opinion cases in veterinary practices in Cambridgeshire. Sixteen cats were dead on arrival; the mortality rate for the remaining cats was 16 per cent. Half of the cats were aged between seven months and two years, with more males than females affected. Most cats had moderate injuries; strays had more severe injuries than owned cats. Areas of the body most often injured were the extremities, head and neck, pelvis and thorax. Skeletal injuries were present in 67 cats and neurological signs in 29. Diagnostic procedures and medical treatment were necessary for the majority of cats; surgery was required in 51 cases. Most cats were hospitalised for between two and seven days and some required up to one month of treatment. The cost of treatment was less than £400 for 84 per cent of cats. [source] Selective death of newborn neurons in hippocampal dentate gyrus following moderate experimental traumatic brain injuryJOURNAL OF NEUROSCIENCE RESEARCH, Issue 10 2008Xiang Gao Abstract Memory impairment is one of the most significant residual deficits following traumatic brain injury (TBI) and is among the most frequent complaints heard from patients and their relatives. It has been reported that the hippocampus is particularly vulnerable to TBI, which results in hippocampus-dependent cognitive impairment. There are different regions in the hippocampus, and each region is composed of different cell types, which might respond differently to TBI. However, regional and cell type-specific neuronal death following TBI is not well described. Here, we examined the distribution of degenerating neurons in the hippocampus of the mouse brain following controlled cortical impact (CCI) and found that the majority of degenerating neurons observed were in the dentate gyrus after moderate (0.5 mm cortical deformation) CCI-TBI. In contrast, there were only a few degenerating neurons observed in the hilus, and we did not observe any degenerating neurons in the CA3 or CA1 regions. Among those degenerating cells in the dentate gyrus, about 80% of them were found in the inner granular neuron layer. Analysis with cell type-specific markers showed that most of the degenerating neurons in the inner granular neuron layer are newborn immature neurons. Further quantitative analysis shows that the number of newborn immature neurons in the dentate gyrus is dramatically decreased in the ipsilateral hemisphere compared with the contralateral side. Collectively, our data demonstrate the selective death of newborn immature neurons in the hippocampal dentate gyrus following moderate injury with CCI in mice. This selective vulnerability of newborn immature dentate neurons may contribute to the persistent impairment of learning and memory post-TBI and provide an innovative target for neuroprotective treatment strategies. © 2008 Wiley-Liss, Inc. [source] Fasting is neuroprotective following traumatic brain injury,JOURNAL OF NEUROSCIENCE RESEARCH, Issue 8 2008Laurie M. Davis Abstract To determine the neuroprotective effect of fasting after traumatic brain injury (TBI) and to elucidate the potential underlying mechanisms, we used a controlled cortical impact (CCI) injury model to induce either a moderate or a severe injury to adult male Sprague Dawley rats. Tissue-sparing assessments were used to determine the level of neuroprotection of fasting, hypoglycemia (insulin 10 U), or ketone (1.66 mmoles/kg/day or 0.83 mmoles/kg/day; D-beta-hydroxtbutyrate) administration. Mitochondrial isolation and respiratory studies were utilized to determine the functionality of mitochondria at the site of injury. We also investigated biomarkers of oxidative stress, such as lipid/protein oxidation, reactive oxygen species (ROS) production, and intramitochondrial calcium load, as a secondary measure of mitochondrial homeostasis. We found that fasting animals for 24 hr, but not 48 hr, after a moderate (1.5 mm), but not severe (2.0 mm), CCI resulted in a significant increase in tissue sparing. This 24-hr fast also decreased biomarkers of oxidative stress and calcium loading and increased mitochondrial oxidative phosphorylation in mitochondria isolated from the site of injury. Insulin administration, designed to mimic the hypoglycemic effect seen during fasting did not result in significant tissue sparing after moderate CCI injury and in fact induced increased mortality at some injection time points. However, the administration of ketones resulted in increased tissue sparing after moderate injury. Fasting for 24 hr confers neuroprotection, maintains cognitive function, and improves mitochondrial function after moderate (1.5 mm) TBI. The underlying mechanism appears to involve ketosis rather than hypoglycemia. © 2008 Wiley-Liss, Inc. [source] Clinical Implications of Hepatic Preservation Injury After Adult Liver TransplantationAMERICAN JOURNAL OF TRANSPLANTATION, Issue 8 2003Matthias Glanemann Several advances in organ preservation have allowed for improved results after liver transplantation; however, little information is available regarding the clinical impact of preservation injury on the postoperative course. The medical records of 889 liver transplants were retrospectively reviewed. Preservation injury was classified according to postoperative aspartate aminotransferase values as minor (<1000 U/L), moderate (1000,5000 U/L), or severe (>5000 U/L). The following criteria were analyzed and compared according to the extent of preservation injury: patient and graft survival, retransplantation rate, duration of hospitalization and postoperative ventilation, as well as incidence of rejection, infection, and hemodialysis. The majority of patients received a liver with minor preservation injury (75.9%), whereas 22.7% and 1.3% of grafts showed moderate or severe injury. Graft survival was significantly lower in patients with severe preservation injury, when compared to minor or moderate injury. The relative risk for initial nonfunction was 39.36-fold increased (95% confidence interval (ci): 10.3,150.2), as it was increased for duration of postoperative ventilation (6.92-fold; 95%ci: 2.1,22.3) and hemodialysis (6.13-fold; 95%ci: 1.9,19.3). Since the incidence of retransplantation was significantly increased (50%), patient survival remained comparable between all groups. Severe preservation injury had a tremendous impact on the postoperative clinical course, requiring the maximum medical effort to achieve adequate patient survival. [source] Trauma Center Utilization for Children in California 1998,2004: Trends and Areas for Further AnalysisACADEMIC EMERGENCY MEDICINE, Issue 4 2007N. Ewen Wang MD Abstract Background: While it is known that trauma systems improve the outcome of injury in children, there is a paucity of information regarding trauma system function amid changes in policies and health care financing that affect emergency medical systems for children. Objectives: To describe the trends in the proportion of pediatric trauma patients acutely hospitalized in trauma-designated versus non,trauma-designated hospitals. Methods: This was a retrospective observational study of a population-based cohort obtained by secondary analysis of a publicly available data set: the California Office of Statewide Health Planning and Development Patient Discharge Database from 1998 to 2004. Patients were included in the analysis if they were 0,19 years old, had International Classification of Disease, Ninth Revision (ICD-9) diagnostic codes and E-codes indicative of trauma, had an unscheduled admission, and were discharged from a general acute care hospital (N= 111,566). Proportions of patients hospitalized in trauma-designated hospitals versus non,trauma-designated hospitals were calculated for Injury Severity Score and death. Injury Severity Scores were calculated from ICD-9 codes. Primary outcomes were hospitalization in a trauma center and death two or more days after hospitalization. Results: Over the study period, the proportion of children aged 0,14 years with acute trauma requiring hospitalization and who were cared for in trauma-designated hospitals increased from 55% (95% confidence interval [CI] = 54% to 56%) in 1998 to 66% (95% CI = 65% to 67%) in 2004 (p < 0.01). For children aged 15,19 years, the proportion increased from 55% (95% CI = 54% to 57%) in 1998 to 74% (95% CI = 72% to 75%) in 2004 (p < 0.0001). When trauma discharges were stratified by injury severity, the proportion of children with severe injury who were hospitalized in trauma-designated hospitals increased from 69% (95% CI = 66% to 72%) in 1998 to 84% (95% CI = 82% to 87%) in 2004, a rate higher than in children with moderate injury (59% [95% CI = 58% to 61%] in 1998 and 75% [95% CI = 74% to 76%] in 2004) and mild injury (51% [95% CI = 50% to 52%] in 1998 and 63% [95% CI = 62% to 64%] in 2004) (p < 0.0001 for each injury severity category and both age groups). Of the hospitalized children who died two or more days after injury (n= 502), 18.1% died in non,trauma-designated hospitals (p < 0.002 for children aged 0,14 years; p = 0.346 for children aged 15,19 years). Conclusions: An increasing majority of children with trauma were cared for in trauma-designated hospitals over the study period. However, 23% of children with severe injuries, and 18.1% of pediatric deaths more than two days after injury, were cared for in non,trauma-designated hospitals. These findings demonstrate an important opportunity for improvement. If we can characterize those children who do not access the trauma system despite severe injury or death, we will be able to design clinical protocols and implement policies that ensure access to appropriate regional trauma care for all children in need. [source] | ||||||||||