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Journal articles on the topic 'Major traumatic injury'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Cole, Elaine, Antonia Lynch, Jackie Bridges, and Anita West. "Older people and major trauma." Reviews in Clinical Gerontology 19, no. 2 (May 2009): 77–85. http://dx.doi.org/10.1017/s0959259809990177.

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SummaryMajor traumatic injury is a leading cause of death in younger age groups, but increasingly older people are affected also. Adverse outcomes, both physical and psychological, are associated with injury in the older population. This review aims to locate and describe the evidence relating to older people and major trauma in order to inform policy, practice, research and education. The published research and systematic reviews fall into three main topics: mechanism of traumatic injury in older people, the effects of co-morbidities on older trauma patients and outcomes following serious traumatic injury in older people. The psychological impact of traumatic injury and the resulting functional alteration cannot be underestimated in this group of patients.

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2

Herman, Carl D. "Major depression following traumatic brain injury." Journal of Head Trauma Rehabilitation 19, no. 4 (2004): 349. http://dx.doi.org/10.1097/00001199-200407000-00010.

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3

Jorge, Ricardo E., Robert G. Robinson, David Moser, Amane Tateno, Benedicto Crespo-Facorro, and Stephan Arndt. "Major Depression Following Traumatic Brain Injury." Archives of General Psychiatry 61, no. 1 (January 1, 2004): 42. http://dx.doi.org/10.1001/archpsyc.61.1.42.

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4

Finnie, J. W., and P. C. Blumbergs. "Traumatic Brain Injury." Veterinary Pathology 39, no. 6 (November 2002): 679–89. http://dx.doi.org/10.1354/vp.39-6-679.

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Animal models have played a critical role in elucidating the complex pathogenesis of traumatic brain injury, the major cause of death and disability in young adults in Western countries. This review discusses how different types of animal models are useful for the study of neuropathologic processes in traumatic, blunt, nonmissile head injury.

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5

Powelson, Elisabeth B., Brianna Mills, William Henderson-Drager, Millie Boyd, Monica S. Vavilala, and Michele Curatolo. "Predicting chronic pain after major traumatic injury." Scandinavian Journal of Pain 19, no. 3 (July 26, 2019): 453–64. http://dx.doi.org/10.1515/sjpain-2019-0040.

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Abstract Background and aims Chronic pain after traumatic injury and surgery is highly prevalent, and associated with substantial psychosocial co-morbidities and prolonged opioid use. It is currently unclear whether predicting chronic post-injury pain is possible. If so, it is unclear if predicting chronic post-injury pain requires a comprehensive set of variables or can be achieved only with data available from the electronic medical records. In this prospective study, we examined models to predict pain at the site of injury 3–6 months after hospital discharge among adult patients after major traumatic injury requiring surgery. Two models were developed: one with a comprehensive set of predictors and one based only on variables available in the electronic medical records. Methods We examined pre-injury and post-injury clinical variables, and clinical management of pain. Patients were interviewed to assess chronic pain, defined as the presence of pain at the site of injury. Prediction models were developed using forward stepwise regression, using follow-up surveys at 3–6 months. Potential predictors identified a priori were: age; sex; presence of pre-existing chronic pain; intensity of post-operative pain at 6 h; in-hospital opioid consumption; injury severity score (ISS); location of trauma, defined as body region; use of regional analgesia intra- and/or post-operatively; pre-trauma PROMIS Depression, Physical Function, and Anxiety scores; in-hospital Widespread Pain Index and Symptom Severity Score; and number of post-operative non-opioid medications. After the final model was developed, a reduced model, based only on variables available in the electronic medical record was run to understand the “value add” of variables taken from study-specific instruments. Results Of 173 patients who completed the baseline interview, 112 completed the follow-up within 3–6 months. The prevalence of chronic pain was 66%. Opioid use increased from 16% pre-injury to 28% at 3–6 months. The final model included six variables, from an initial set of 24 potential predictors. The apparent area under the ROC curve (AUROC) of 0.78 for predicting pain 3–6 months was optimism-corrected to 0.73. The reduced final model, using only data available from the electronic health records, included post-surgical pain score at 6 h, presence of a head injury, use of regional analgesia, and the number of post-operative non-opioid medications used for pain relief. This reduced model had an apparent AUROC of 0.76, optimism-corrected to 0.72. Conclusions Pain 3–6 months after trauma and surgery is highly prevalent and associated with an increase in opioid use. Chronic pain at the site of injury at 3–6 months after trauma and surgery may be predicted during hospitalization by using routinely collected clinical data. Implications If our model is validated in other populations, it would provide a tool that can be easily implemented by any provider with access to medical records. Patients at risk of developing chronic pain could be selected for studies on preventive strategies, thereby concentrating the interventions to patients who are most likely to transition to chronic pain.

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Taber, Katherine H., and Robin A. Hurley. "Traumatic Axonal Injury: Atlas of Major Pathways." Journal of Neuropsychiatry and Clinical Neurosciences 19, no. 2 (April 2007): iv—104. http://dx.doi.org/10.1176/jnp.2007.19.2.iv.

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7

Chambers, M. G., C. M. Airey, S. Chell, A. S. Rigby, J. Connelly, and A. Tennant. "A cost analysis of major traumatic injury." Injury 27, no. 5 (June 1996): 369. http://dx.doi.org/10.1016/0020-1383(96)86852-5.

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8

Thombs, Brett D. "Traumatic Brain Injury and Major Depressive Disorder." JAMA 304, no. 8 (August 25, 2010): 857. http://dx.doi.org/10.1001/jama.2010.1170.

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9

van Leeuwen, Nikki, Hester F. Lingsma, Pablo Perel, Fiona Lecky, Bob Roozenbeek, Juan Lu, Haleema Shakur, James Weir, Ewout W. Steyerberg, and Andrew I. R. Maas. "Prognostic Value of Major Extracranial Injury in Traumatic Brain Injury." Neurosurgery 70, no. 4 (April 2012): 811–18. http://dx.doi.org/10.1227/neu.0b013e318235d640.

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10

Khatri, Nidhi, Manisha Thakur, Vikas Pareek, Sandeep Kumar, Sunil Sharma, and Ashok Kumar Datusalia. "Oxidative Stress: Major Threat in Traumatic Brain Injury." CNS & Neurological Disorders - Drug Targets 17, no. 9 (November 2, 2018): 689–95. http://dx.doi.org/10.2174/1871527317666180627120501.

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Background & Objective: Traumatic Brain Injury (TBI) is one of the major causes of mortality and morbidity worldwide. It represents mild, moderate and severe effects of physical assault to brain which may cause sequential, primary or secondary ramifications. Primary injury can be due to the first physical hit, blow or jolt to one of the brain compartments. The primary injury is then followed by secondary injury which leads to biochemical, cellular, and physiological changes like blood brain barrier disruption, inflammation, excitotoxicity, necrosis, apoptosis, mitochondrial dysfunction and generation of oxidative stress. Apart from this, there is also an immediate increase in glutamate at the synapses following severe TBI. Excessive glutamate at synapses in turn activates corresponding NMDA and AMPA receptors that facilitate excessive calcium influx into the neuronal cells. This leads to the generation of oxidative stress which further leads to mitochondrial dysfunction, lipid peroxidation and oxidation of proteins and DNA. As a consequence, neuronal cell death takes place and ultimately people start facing some serious disabilies. Conclusion: In the present review we provide extensive overview of the role of reactive oxygen species (ROS)-induced oxidative stress and its fatal effects on brain after TBI.

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11

Hart, Tessa, Lisa Brenner, Allison N. Clark, Jennifer A. Bogner, Thomas A. Novack, Inna Chervoneva, Risa Nakase-Richardson, and Juan Carlos Arango-Lasprilla. "Major and Minor Depression After Traumatic Brain Injury." Archives of Physical Medicine and Rehabilitation 92, no. 8 (August 2011): 1211–19. http://dx.doi.org/10.1016/j.apmr.2011.03.005.

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12

Bombardier, Charles H. "Traumatic Brain Injury and Major Depressive Disorder—Reply." JAMA 304, no. 8 (August 25, 2010): 857. http://dx.doi.org/10.1001/jama.2010.1171.

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13

Bade-Boon, Jordan, Joseph K. Mathew, Mark C. Fitzgerald, and Biswadev Mitra. "Traumatic aortic injury presenting to an adult major trauma centre." Trauma 21, no. 4 (June 6, 2018): 272–79. http://dx.doi.org/10.1177/1460408618773547.

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Introduction Traumatic aortic injury is an uncommon condition. Timely diagnosis may enable early haemostatic resuscitation, essential to prevent worsening of the injury prior to definitive management. The aim of this study was to assess the utility of initial vital signs and presenting clinical characteristics to confirm or rule out aortic injury. Methods A retrospective review of patients from The Alfred Trauma Registry was conducted. Patients presenting between January 2006 and July 2014 and diagnosed with aortic injury were identified. Demographics and presenting clinical characteristics were extracted. Sensitivity of individual clinical variables for the detection of aortic injury was calculated. Results There were 77 patients identified with aortic injury, with an in-hospital mortality rate of 19.5% (95% CI: 10.6–28.3%). Of these, 68 (88.3%) patients presented after high-energy blunt mechanisms. Clinical signs and early chest X-ray findings were poorly sensitive to detect aortic injury. Patients who presented with hypotension had a greater severity of aortic injury, more commonly had associated abnormal investigation findings and were more likely to require blood products and inotropic agents (p < 0.05). However, sensitivity of initial hypotension to rule out aortic injury was 39.0% (95% CI: 28.1–49.9%). Conclusions The diagnosis of aortic injury was uncommon in hospital. Most injuries were secondary to high-velocity road traffic crashes or high falls. Clinical signs were not adequately sensitive to be used for the exclusion of aortic injury. We recommend a high degree of clinical suspicion and liberal imaging among cases where aortic injury is possible.

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14

Rapoport, Mark J., Scott McCullagh, David Streiner, and Anthony Feinstein. "Age and Major Depression After Mild Traumatic Brain Injury." American Journal of Geriatric Psychiatry 11, no. 3 (May 2003): 365–69. http://dx.doi.org/10.1097/00019442-200305000-00015.

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15

McFarlane, Alexander C. "PREDICTORS OF POST-TRAUMATIC STRESS DISORDER AFTER MAJOR INJURY." ANZ Journal of Surgery 78, no. 7 (July 2008): 533–34. http://dx.doi.org/10.1111/j.1445-2197.2008.04566.x.

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16

Jorge, Ricardo E., and Sergio E. Starkstein. "Pathophysiologic Aspects of Major Depression Following Traumatic Brain Injury." Journal of Head Trauma Rehabilitation 20, no. 6 (November 2005): 475–87. http://dx.doi.org/10.1097/00001199-200511000-00001.

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17

Jesus, D., L. Lima, C. Alves, J. C. Fernandes, G. Fernandes, and B. Jardim. "Major depression and suicidal ideation following traumatic brain injury." Annals of Physical and Rehabilitation Medicine 57 (May 2014): e72. http://dx.doi.org/10.1016/j.rehab.2014.03.260.

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18

DAVIS, RICHARD F. "Acute Renal Failure Following Traumatic Injury or Major Operation." International Anesthesiology Clinics 25, no. 1 (1987): 117–42. http://dx.doi.org/10.1097/00004311-198702510-00009.

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19

Skelton, C. E., R. M. Walley, J. B. Chisholm, and R. L. Sloan. "Mild Traumatic Brain Injury — the Fife Perspective." Scottish Medical Journal 42, no. 2 (April 1997): 40–43. http://dx.doi.org/10.1177/003693309704200204.

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Results are reported from a study to identify patients residing in Fife with mild traumatic brain injury in the 16–65 year old age group, who attended an accident and emergency department following their brain injury. Over a two month period 161 such patients attended with minor head trauma, of which 33 entered our study. The major cause of mild traumatic brain injury was assault. We found that over two-thirds of patients in the study had persisting post-concussive symptoms six months post injury. Neuropsychological testing showed problems of concentration and memory, but not at a level that was significantly different from that expected in an average population. Other studies have shown that symptom rates are higher when patients get no explanation of their symptoms and we feel that better co-ordination of services for brain injured patients in Fife is required, to provide the necessary information, education and support.

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20

Dade, Nagendra Babu, Ramesh Teegala, and Meena Medikonda. "Study of Epidemiology of Traumatic Brain Injury and Prevalence of Psychiatric Disorders in Traumatic Brain Injury at 3 Months Follow-Up." Nepal Journal of Neuroscience 16, no. 2 (October 16, 2019): 8–15. http://dx.doi.org/10.3126/njn.v16i2.25939.

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Traumatic brain injury (TBI) is a major global health problem with an annual incidence of 10million cases globally. Despite the good recovery with modern treatment measures, the cognitive and behavioral deficits give rise to the major morbidity. These deficits amount in failure to return to work and maintain social activities. A prospective clinical study of 187 inpatients with Traumatic Brain Injury was done in Alluri Sitarama Raju Academy of Medical Sciences, Eluru, Andhra Pradesh from August 2015 to August 2017. All patients aged between 15-60years, with normal premorbid personality admitted with traumatic brain injury, were included in the study. Appropriate socio-demographic and clinical data was collected while inpatient, and 3 months post trauma. All the patients were subjected to structured interview using MINI PLUS (English version 5.0.0) for assessment of cognitive and neurobehavioral disorders. The prevalence of cognitive and neurobehavioural disorders following traumatic brain injury in the present study was40.6%.Patients with traumatic brain injury often experience enduring emotional and cognitive consequences; major depressive disorder being the most common, followed by somatoform and anxiety disorders. Treatment of these patients should involve a multidisciplinary approach, with the psychiatrist working in close collaboration with the patient, family, neurologist/neurosurgeon, psychologist and social worker.

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21

Fesharaki-Zadeh, Arman. "Oxidative Stress in Traumatic Brain Injury." International Journal of Molecular Sciences 23, no. 21 (October 27, 2022): 13000. http://dx.doi.org/10.3390/ijms232113000.

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Traumatic Brain Injury (TBI) remains a major cause of disability worldwide. It involves a complex neurometabolic cascade, including oxidative stress. The products of this manuscript is examining the underlying pathophysiological mechanism, including reactive oxygen species (ROS) and reactive nitrogen species (RNS). This process in turn leads to secondary injury cascade, which includes lipid peroxidation products. These reactions ultimately play a key role in chronic inflammation and synaptic dysfunction in a synergistic fashion. Although there are no FDA approved antioxidant therapy for TBI, there is a number of antioxidant therapies that have been tested and include free radical scavengers, activators of antioxidant systems, inhibitors of free radical generating enzymes, and antioxidant enzymes. Antioxidant therapies have led to cognitive and functional recovery post TBI, and they offer a promising treatment option for patients recovering from TBI. Current major challenges in treatment of TBI symptoms include heterogenous nature of injury, as well as access to timely treatment post injury. The inherent benefits of antioxidant therapies include minimally reported side effects, and relative ease of use in the clinical setting. The current review also provides a highlight of the more studied anti-oxidant regimen with applicability for TBI treatment with potential use in the real clinical setting.

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22

Weber, Christian D., Rolf Lefering, Richard M. Sellei, Klemens Horst, Filippo Migliorini, and Frank Hildebrand. "Traumatic Hip Dislocations in Major Trauma Patients: Epidemiology, Injury Mechanisms, and Concomitant Injuries." Journal of Clinical Medicine 11, no. 3 (January 18, 2022): 472. http://dx.doi.org/10.3390/jcm11030472.

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Introduction: Traumatic hip dislocations (THDs) are severe injuries associated with considerable morbidity. Delayed recognition of fracture dislocations and neurovascular deficits have been proposed to cause deleterious long-term clinical outcomes. Therefore, in this study, we aimed to identify characteristics of epidemiology, injury mechanisms, and associated injuries to identify patients at risk. Methods: For this study based on the TraumaRegister DGU® (January 2002–December 2017), the inclusion criterion was an Injury Severity Score (ISS) ≥9 points. Exclusion criteria were an isolated head injury and early transfer to another hospital. The THD group was compared to a control group without hip dislocation. The ISS and New ISS were used for injury severity and the Abbreviated Injury Scale for associated injuries classification. Univariate and logistic regression analyses were performed. Results: The final study cohort comprised n = 170,934 major trauma patients. We identified 1359 individuals (0.8%) with THD; 12 patients had sustained bilateral hip dislocations. Patients with THD were predominantly male (79.5%, mean age 43 years, mean ISS 22.4 points). Aortic injuries (2.1% vs. 0.9%, p ≤ 0.001) were observed more frequently in the THD group. Among the predictors for THDs were specific injury mechanisms, including motor vehicle accidents (odds ratio (OR) 2.98, 95% confidence interval (CI) 2.57–3.45, p ≤ 0.001), motorcycle accidents (OR 1.99, 95% CI 1.66–2.39, p ≤ 0.001), and suicide attempts (OR 1.36, 95% CI 1.06–1.75, p = 0.016). Despite a lower rate of head injuries and a comparable level of care measured by trauma center admission, both intensive care unit and total hospital stay were prolonged in patients with THD. Conclusions: Since early diagnosis, as well as timely and sufficient treatment, of THDs are of high relevance for long-term outcomes of severely injured individuals, knowledge of patients at risk for this injury pattern is of utmost importance. THDs are frequently related to high-energy mechanisms and associated with severe concomitant injuries in major trauma patients.

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Vaid, Parul, Bhavuk Kapoor, and Mayank Kapoor. "Epidemiology of surgically managed traumatic brain injury patients." IP Indian Journal of Anatomy and Surgery of Head, Neck and Brain 7, no. 4 (January 15, 2022): 99–102. http://dx.doi.org/10.18231/j.ijashnb.2021.026.

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Traumatic brain injury (TBI) constitutes a major health and socioeconomic problem throughout the world TBI is called the ‘silent epidemic’ because problems resulting from TBI are often not immediately visible and TBI patients are not very vociferous. Epidemiological studies of TBI are essential to the targeted prevention and effective treatment of brain-injured patients. Epidemiology analysis of surgically managed traumatic brain injury patients was done. Mean age was 35.9 years. Males were more commonly (80%) involved than females (20%). In 57.5% of cases, falls were responsible for TBI and in 42.5% of cases, Road traffic accidents were responsible. Edh was the most common type of TBI in (50%). Chronic SDH occurred in 25% of cases. Acute SDH and Contusions were both seen in 13.75% of cases. Depressed fractures occurred in 6.25% of cases and ICH occurred in 1.25% of cases. Craniotomy was the most common (42%) surgical procedure performed, followed by burrhole drainage (22.5%). Decompressive craniectomy was done in 18.75% of cases and elevation of depressed fracture was performed in 6.25% of cases. Traumatic brain injury (TBI) constitutes a major health and socioeconomic problem throughout the world. People of all ages are affected by it. Males are more commonly involved as compared to females. Timely hospitalisation and surgical management whenever indicated improves the survival.

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Lu, Rommel P., Ai Ni, Feng-Chang Lin, Shiara M. Ortiz-Pujols, Sasha D. Adams, Dougald M. Monroe, Herbert C. Whinna, Bruce A. Cairns, and Nigel S. Key. "Major burn injury is not associated with acute traumatic coagulopathy." Journal of Trauma and Acute Care Surgery 74, no. 6 (June 2013): 1474–79. http://dx.doi.org/10.1097/ta.0b013e3182923193.

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25

Oquendo, Maria A., Jill Harkavy Friedman, Michael F. Grunebaum, Ainsley Burke, Jonathan M. Silver, and J. John Mann. "Suicidal Behavior and Mild Traumatic Brain Injury in Major Depression." Journal of Nervous and Mental Disease 192, no. 6 (June 2004): 430–34. http://dx.doi.org/10.1097/01.nmd.0000126706.53615.7b.

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26

Kieltyka, J., D. Kyriacou, and M. Crandall. "Predicting the Daily Incidence of Major Traumatic Injury in Chicago." Journal of Surgical Research 172, no. 2 (February 2012): 200. http://dx.doi.org/10.1016/j.jss.2011.11.239.

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Gaither, Joshua B., Sophie Galson, Merlin Curry, Moses Mhayamaguru, Christopher Williams, Samuel M. Keim, Bentley J. Bobrow, and Daniel W. Spaite. "Environmental Hyperthermia in Prehospital Patients with Major Traumatic Brain Injury." Journal of Emergency Medicine 49, no. 3 (September 2015): 375–81. http://dx.doi.org/10.1016/j.jemermed.2015.01.038.

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28

Airey, C. M., S. Chell, A. S. Rigby, M. Chambers, A. Tennant, and J. Connelly. "The prevalence of disability among survivors of major traumatic injury." Injury 27, no. 5 (June 1996): 368. http://dx.doi.org/10.1016/0020-1383(96)86850-1.

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29

Karakaya, Dicle, and Ahmet İlkay Işıkay. "A Review of Traumatic Axonal Injury." Acta Medica 52, no. 2 (June 20, 2021): 102–8. http://dx.doi.org/10.32552/2021.actamedica.467.

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Traumatic brain injury is a major cause of mortality and neurological disability worldwide and varies according to its cause, pathogenesis, severity and clinical outcome. This review summarizes a significant aspect of diffuse brain injuries – traumatic axonal injury – important cause of severe disability and vegetative state. Traumatic axonal injury is a type of traumatic brain injury caused by blunt head trauma. It is defined both clinically (immediate and prolonged unconsciousness, characteristically in the absence of space-occupying lesions) and pathologically (widespread and diffuse damage of axons). Following traumatic brain injury, progressive axonal degeneration starts with disruption of axonal transport, axonal swelling, secondary axonal disconnection and Wallerian degeneration, respectively. However, traumatic axonal injury is difficult to define clinically, it should be considered in patients with Glasgow coma score < 8 for more than six hours after trauma and diffuse tensor imaging and sensitivity-weighted imaging MRI sequences are highly sensitive in its diagnosis. Glasgow coma score at the time of presentation, location and severity of axonal damage are prognostic factors for clinical outcome.

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30

Stiver, Shirley I., and Geoffrey T. Manley. "Prehospital management of traumatic brain injury." Neurosurgical Focus 25, no. 4 (October 2008): E5. http://dx.doi.org/10.3171/foc.2008.25.10.e5.

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The aim of this study was to review the current protocols of prehospital practice and their impact on outcome in the management of traumatic brain injury. A literature review of the National Library of Medicine encompassing the years 1980 to May 2008 was performed. The primary impact of a head injury sets in motion a cascade of secondary events that can worsen neurological injury and outcome. The goals of care during prehospital triage, stabilization, and transport are to recognize life-threatening raised intracranial pressure and to circumvent cerebral herniation. In that process, prevention of secondary injury and secondary insults is a major determinant of both short- and longterm outcome. Management of brain oxygenation, blood pressure, cerebral perfusion pressure, and raised intracranial pressure in the prehospital setting are discussed. Patient outcomes are dependent upon an organized trauma response system. Dispatch and transport timing, field stabilization, modes of transport, and destination levels of care are addressed. In addition, special considerations for mass casualty and disaster planning are outlined and recommendations are made regarding early response efforts and the ethical impact of aggressive prehospital resuscitation. The most sophisticated of emergency, operative, or intensive care units cannot reverse damage that has been set in motion by suboptimal protocols of triage and resuscitation, either at the injury scene or en route to the hospital. The quality of prehospital care is a major determinant of long-term outcome for patients with traumatic brain injury.

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Parabucki, Ana, Danijela Savic, Danijela Laketa, Sanja Pekovic, Mirjana Stojiljkovic, Nadezda Nedeljkovic, and Ivana Bjelobaba. "Expression of major ectonucleotidases after cortical stab brain injury in rats: A real-time PCR study." Archives of Biological Sciences 66, no. 1 (2014): 149–55. http://dx.doi.org/10.2298/abs1401148p.

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Ectonucleotidases are cell surface-located enzymes responsible for the extracellular degradation of nucleotides. They are comprised of several protein families: ectonucleoside triphosphate diphosphohydrolases (E-NTPDase), ectonucleotide pyrophosphatase/phosphodiesterases (E-NPPases) and ecto-5?-nucleotidase. Previously we showed that cortical stab injury alters ectonucleotidase activities in the rat brain, but that the specific enzymes responsible for these changes were not identified. In this study we investigated the gene expression of the specific ectonucleotidase enzymes, NTPDase1- 3, NPP1-3 and ecto-5?-nucleotidase, two and seven days after cortical stab injury in rats, using real-time PCR. Two days after the injury we observed only one significant change: the downregulation in NTPDase2 mRNA expression. Our results indicate that traumatic brain injury induces significant upregulation of NTPDase1, NTPDase2 and ecto-5?-nucleotidase transcripts, and the downregulation of NPP1, seven days after the injury. Thus, traumatic brain injury has diverse impacts on ectonucleotidases gene expression, which may be reflected in the enzyme activities and extracellular nucleotide concentrations in the perilesional tissue.

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Turchan, Agus, Alivery Raihanada Armando, Meisy Andriana, and Martha Kurnia Kusumawardani. "An Overview of the Quality of Life of Post Severe Brain Injury Patients within 2018-2020 Period of Time in Dr. Soetomo General Academic Hospital based on Short Form-36." AKSONA 2, no. 2 (July 31, 2022): 62–71. http://dx.doi.org/10.20473/aksona.v2i2.35816.

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Highlight: Until today, Traumatic Brain Injury is still a major cause of death, disability, and a serious health issue Traumatic Brain Injury patients have a good quality of life if they get adequate therapy and on time interventions ABSTRACT Introduction: Approximately 90 million traumatic brain injury (TBI) cases worldwide exist yearly. TBI pathophysiology varies, which may cause diverse complications. These complications may decrease the patients’ quality of life. Objective: Describing the quality of life of traumatic brain-injured patients after being treated at Dr. Soetomo General Academic Hospital Period 2018-2020. Methods: This research is a descriptive cross-sectional study using SF-36 questionnaire data from patients with post-severe brain injury at Dr. Soetomo General Academic Hospital in 2018-2020. Results: The value of the physical component (59.9) and mental component (68.6) in patients with severe brain injury at Dr. Soetomo General Academic Hospital showed a good quality of life, with values in the SF-36 domains, namely physical function (58.2), physical limitations (46.7), body pain (73.6), general health (61.3), vitality (65.3), social functioning (72.5), emotional limitations (60), and mental health (76.5) is above the threshold value (50) except for physical limitations (46.7).Conclusion: Patients with severe brain injury had a good quality of life after receiving treatment in Dr. Soetomo General Academic Hospital.

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Zhu, Dexiao, Fei Gao, and Chu Chen. "Endocannabinoid Metabolism and Traumatic Brain Injury." Cells 10, no. 11 (November 2, 2021): 2979. http://dx.doi.org/10.3390/cells10112979.

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Traumatic brain injury (TBI) represents a major cause of morbidity and disability and is a risk factor for developing neurodegenerative diseases, including Alzheimer’s disease (AD). However, no effective therapies are currently available for TBI-induced AD-like disease. Endocannabinoids are endogenous lipid mediators involved in a variety of physiological and pathological processes. The compound 2-arachidonoylglycerol (2-AG) is the most abundant endocannabinoid with profound anti-inflammatory and neuroprotective properties. This molecule is predominantly metabolized by monoacylglycerol lipase (MAGL), a key enzyme degrading about 85% of 2-AG in the brain. Studies using animal models of inflammation, AD, and TBI provide evidence that inactivation of MAGL, which augments 2-AG signaling and reduces its metabolites, exerts neuroprotective effects, suggesting that MAGL is a promising therapeutic target for neurodegenerative diseases. In this short review, we provide an overview of the inhibition of 2-AG metabolism for the alleviation of neuropathology and the improvement of synaptic and cognitive functions after TBI.

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Klein, Deborah Goldenberg. "Physiologic Response to Traumatic Shock." AACN Advanced Critical Care 1, no. 3 (November 1, 1990): 505–21. http://dx.doi.org/10.4037/15597768-1990-3006.

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Traumatic injury results in major physiologic alterations that begin at the time of injury and persist until recovery is complete. The response of the body is divided into two phases — the acute phase and the flow phase. The acute phase is characterized by shock with changes in hormone concentration. These hormones, either alone or in combination, result in lipolysis, amino acid release, gluconeogenesis, and glycolysis. The flow phase of injury is a catabolic process that is characterized by an increased protein metabolism. Hypermetabolism and increased nitrogen losses are seen. The magnitude of these alterations is directly related to the severity of injury. Tissues with the highest oxygen consumption are more susceptible to injury and death. Cellular function does not depend on oxygen alone but also on the ability of the cells to use available oxygen. If the body is unable to compensate through biochemical, hormonal, and metabolic activities, an irreversible state results unless appropriate interventions are instituted promptly

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Stein, Sherman C., Xiao-Han Chen, Grant P. Sinson, and Douglas H. Smith. "Intravascular coagulation: a major secondary insult in nonfatal traumatic brain injury." Journal of Neurosurgery 97, no. 6 (December 2002): 1373–77. http://dx.doi.org/10.3171/jns.2002.97.6.1373.

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Object. The goal of this study was to determine the frequency with which cerebral intravascular coagulation (IC) complicates traumatic brain injury (TBI). The authors also investigated the incidence of IC in relation to varying mechanisms, time courses, and severities of TBI and in different species. Methods. Tissue was sampled from surgical specimens of human cerebral contusions, from rats with lateral fluid-percussion injuries, and from pigs with head rotational acceleration injuries. Immunohistochemical fluorescent staining for antithrombin III was performed to detect cerebral intravascular microthrombi. Abundant IC was found in all specimens, and microthrombi had formed in arterioles and venules of all sizes, ranging from 10 to 600 µm. Although it was more pronounced in focal lesions and more severe injuries, considerable IC was also observed in mild and diffuse injuries. The authors found a strong association between the severity of coagulopathy and the density of IC. Conclusions. These results strongly support the contention that IC is a universal response to TBI and an important secondary cerebral insult.

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Fann, Jesse R., Charles H. Bombardier, Nancy Temkin, Peter Esselman, Catherine Warms, Jason Barber, and Sureyya Dikmen. "Sertraline for Major Depression During the Year Following Traumatic Brain Injury." Journal of Head Trauma Rehabilitation 32, no. 5 (2017): 332–42. http://dx.doi.org/10.1097/htr.0000000000000322.

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Rapoport, Mark J., Scott Mccullagh, David Streiner, and Anthony Feinstein. "The Clinical Significance of Major Depression Following Mild Traumatic Brain Injury." Psychosomatics 44, no. 1 (January 2003): 31–37. http://dx.doi.org/10.1176/appi.psy.44.1.31.

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Chan, Florance, Krista L. Lanctôt, Anthony Feinstein, Nathan Herrmann, John Strauss, Tricia Sicard, James L. Kennedy, Scott McCullagh, and Mark J. Rapoport. "The serotonin transporter polymorphisms and major depression following traumatic brain injury." Brain Injury 22, no. 6 (January 2008): 471–79. http://dx.doi.org/10.1080/02699050802084886.

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Green, Gary A., Keshia M. Pollack, John D’Angelo, Mark S. Schickendantz, Roger Caplinger, Kathleen Weber, Alex Valadka, et al. "Mild Traumatic Brain Injury in Major and Minor League Baseball Players." American Journal of Sports Medicine 43, no. 5 (February 6, 2015): 1118–26. http://dx.doi.org/10.1177/0363546514568089.

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Maller, Jerome J., Richard H. S. Thomson, Philip M. Lewis, Stephen E. Rose, Kerstin Pannek, and Paul B. Fitzgerald. "Traumatic brain injury, major depression, and diffusion tensor imaging: Making connections." Brain Research Reviews 64, no. 1 (September 2010): 213–40. http://dx.doi.org/10.1016/j.brainresrev.2010.04.003.

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Niven, D. J., G. H. Fick, A. W. Kirkpatrick, V. Grant, and K. B. Laupland. "Cost and outcomes of nosocomial bloodstream infections complicating major traumatic injury." Journal of Hospital Infection 76, no. 4 (December 2010): 296–99. http://dx.doi.org/10.1016/j.jhin.2010.06.004.

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Hobson, Mark. "Major traumatic brain injury: how do hypotension and hypoxia affect mortality?" Journal of Paramedic Practice 9, no. 12 (December 2, 2017): 542–44. http://dx.doi.org/10.12968/jpar.2017.9.12.542.

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Tsahakis, James. "Mild traumatic brain injury in major and minor league baseball players." Journal of Emergency Medicine 49, no. 6 (December 2015): 1021. http://dx.doi.org/10.1016/j.jemermed.2015.10.025.

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Alali, Aziz S., David Gomez, Victoria McCredie, Todd G. Mainprize, and Avery B. Nathens. "Understanding Hospital Volume–Outcome Relationship in Severe Traumatic Brain Injury." Neurosurgery 80, no. 4 (January 28, 2017): 534–42. http://dx.doi.org/10.1093/neuros/nyw098.

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Abstract BACKGROUND: The hospital volume–outcome relationship in severe traumatic brain injury (TBI) population remains unclear. OBJECTIVE: To examine the relationship between volume of patients with severe TBI per hospital and in-hospital mortality, major complications, and mortality following a major complication (ie, failure to rescue). METHODS: In a multicenter cohort study, data on 9255 adults with severe TBI were derived from 111 hospitals participating in the American College of Surgeons Trauma Quality Improvement Program over 2009-2011. Hospitals were ranked into quartiles based on their volume of severe TBI during the study period. Random-intercept multilevel models were used to examine the association between hospital quartile of severe TBI volume and in-hospital mortality, major complications, and mortality following a major complication after adjusting for patient and hospital characteristics. In sensitivity analyses, we examined these associations after excluding transferred cases. RESULTS: Overall mortality was 37.2% (n = 3447). Two thousand ninety-eight patients (22.7%) suffered from 1 or more major complication. Among patients with major complications, 27.8% (n = 583) died. Higher-volume hospitals were associated with lower mortality; the adjusted odds ratio of death was 0.50 (95% confidence interval: 0.29-0.85) in the highest volume quartile compared to the lowest. There was no significant association between hospital-volume quartile and the odds of a major complication or the odds of death following a major complication. After excluding transferred cases, similar results were found. CONCLUSION: High-volume hospitals might be associated with lower in-hospital mortality following severe TBI. However, this mortality reduction was not associated with lower risk of major complications or death following a major complication.

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Chittoria, Ravi Kumar, Shivanand Hosamani, and Barath Kumar Singh. "Role of platelet rich fibrin matrix in wound bed preparation in degloving injury." Indian Journal of Orthopaedics Surgery 8, no. 4 (November 15, 2022): 278–81. http://dx.doi.org/10.18231/j.ijos.2022.051.

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Degloving Injury are major debilitating conditions and its treatment is also challenging. The treatment of post traumatic degloving injury requires a multimodal approach. Adjuvant platelet rich fibrin matrix can be tried for post traumatic wounds as a modality for wound bed preparation. In this study we share our experience regarding the use of platelet rich fibrin matrix as an adjunct in the management of post traumatic degloving wounds of the lower extremity.

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Fitri, Nora, Syarif Indra, and Hendra Permana. "Factors Related To Outcome of Traumatic Brain Injury Patients at M Djamil Padang Hospital." Bioscientia Medicina : Journal of Biomedicine and Translational Research 5, no. 8 (July 29, 2021): 811–17. http://dx.doi.org/10.32539/bsm.v5i8.388.

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Background: Traumatic brain injury is still a major threat because it can cause global morbidity and mortality. Many factors can affect the outcome of a traumatic brain injury. Some conditions that can exacerbate traumatic brain injury include GCS conditions, blood pressure variability, and pupillary reflexes.Methods: The research was conducted in M. Djamil Padang Hospital from October 2020 to March 2021. The study design was a cross-sectional study in traumatic brain injury patients with ≤ 48 hours of onset and the aged between 18-60 years. The subjects in this study consisted of 66 subjects. At 6 weeks after onset, a GOS assessment was performed to assess patient outcomes. Statistical analysis was performed computerized with SPSS 22.0. P-value <0.05 was considered statistically significant. Results: Most of the patients were male (71.2%) with an average age of 36.41 ± 14,275 years, and the most common injury mechanism was traffic accidents (95.5%). There was a significant relationship between onset of incidence, hypotension, pupillary reflexes, and Rotterdam score with the outcome of traumatic brain injury patients (p<0.05) and there was no significant relationship between age, gender, and mechanism of injury with the outcome patients with traumatic brain injury. Conclution: The onset of events, hypotension, pupillary reflexes, and Rotterdam scores significantly affect the outcome patients of traumatic brain injury.

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Fitri, Nora, Syarif Indra, and Hendra Permana. "Factors Related To Outcome of Traumatic Brain Injury Patients at M Djamil Padang Hospital." Bioscientia Medicina : Journal of Biomedicine and Translational Research 5, no. 4 (July 29, 2021): 1095–101. http://dx.doi.org/10.32539/bsm.v5i4.388.

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Background: Traumatic brain injury is still a major threat because it can cause global morbidity and mortality. Many factors can affect the outcome of a traumatic brain injury. Some conditions that can exacerbate traumatic brain injury include GCS conditions, blood pressure variability, and pupillary reflexes.Methods: The research was conducted in M. Djamil Padang Hospital from October 2020 to March 2021. The study design was a cross-sectional study in traumatic brain injury patients with ≤ 48 hours of onset and the aged between 18-60 years. The subjects in this study consisted of 66 subjects. At 6 weeks after onset, a GOS assessment was performed to assess patient outcomes. Statistical analysis was performed computerized with SPSS 22.0. P-value <0.05 was considered statistically significant. Results: Most of the patients were male (71.2%) with an average age of 36.41 ± 14,275 years, and the most common injury mechanism was traffic accidents (95.5%). There was a significant relationship between onset of incidence, hypotension, pupillary reflexes, and Rotterdam score with the outcome of traumatic brain injury patients (p<0.05) and there was no significant relationship between age, gender, and mechanism of injury with the outcome patients with traumatic brain injury. Conclution: The onset of events, hypotension, pupillary reflexes, and Rotterdam scores significantly affect the outcome patients of traumatic brain injury.

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Tupetz, Anna, Loren K. Barcenas, Julia E. Isaacson, Joao Ricardo Nickenig Vissoci, Victoria Gerald, Julius Raymond Kingazi, Irene Mushi, et al. "“I Don’t Do Anything; I’m Just Being Taken Care Of”: Experiences of Patients and Their Caregivers Transitioning Back into the Community Following Traumatic Injury in Northern Tanzania." Trauma Care 2, no. 2 (June 3, 2022): 341–58. http://dx.doi.org/10.3390/traumacare2020028.

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After discharge from the hospital for traumatic injury, patients and their caregivers face a period of increased vulnerability. This adjustment phase is poorly characterized, especially in low- and middle-income countries. We explored the experiences of patients and their caregivers in Northern Tanzania after hospitalization for a traumatic injury. Patients who received care for traumatic injury at the Kilimanjaro Christian Medical Center and their caregivers were selected as part of a convenience sample from January 2019 to December 2019. Analysts developed a codebook; content and analytic memos were subsequently created. We then applied the biopsychosocial model to further characterize our findings. Participants included 26 patients and 11 caregivers. Patients were mostly middle-aged (mean age 37.7) males (80.8%), residing in urban settings (57.7%), injured in road traffic accidents (65.4%), and who required surgery (69.2%). Most caregivers were female. Seven major themes arose: pain, decreased physical functioning, poor emotional health, lack of support, challenges with daily activities, financial strain, and obstacles to accessing healthcare. This study describes some of the difficulties transitioning back into the community after hospitalization for traumatic injury. Our work demonstrates the importance of mixed methods approaches in characterizing and addressing transitions of care challenges.

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Zhao, Zilong, Yuan Zhou, Min Li, Jianning Zhang, and Jing-Fei Dong. "Extracellular Mitochondria in Traumatic Brain Injury Induced Coagulopathy." Seminars in Thrombosis and Hemostasis 46, no. 02 (December 30, 2019): 167–75. http://dx.doi.org/10.1055/s-0039-3402427.

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AbstractTraumatic brain injury (TBI) induced coagulopathy remains a significant clinical challenge, with unmet needs for standardizing diagnosis and optimizing treatments. TBI-induced coagulopathy is closely associated with poor outcomes in affected patients. Recent studies have demonstrated that TBI induces coagulopathy, which is mechanistically distinct from the deficient and dilutional coagulopathy found in patients with injuries to the body/limbs and hemorrhagic shock. Multiple causal and disseminating factors have been identified to cause TBI-induced coagulopathy. Among these are extracellular mitochondria (exMTs) released from injured cerebral cells, endothelial cells, and platelets. These circulating exMTs not only express potent procoagulant activity but also promote inflammation, and could remain metabolically active to become a major source of oxidative stress. They activate platelets and endothelial cells to propagate TBI-induced coagulopathy and secondary tissue injury after primary traumatic impact. In this review, we discuss recent advances in our understanding of the role of exMTs in the development of TBI-induced coagulopathy.

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Suherman, Suherman, Ipak Nistriana, and Muhammad Rizky. "AMBARAN FUNGSI MEMORI PADA PASIEN CEDERA KEPALA TRAUMATIK DERAJAT SEDANG DENGAN EDEMA SEREBRI." Jurnal Kedokteran Syiah Kuala 18, no. 2 (August 1, 2018): 80–85. http://dx.doi.org/10.24815/jks.v18i2.17995.

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Abstrak. Latar Belakang Cedera kepala traumatik masih menjadi penyebab utama kecacatan dan kematian di dunia. Sebagian besar terjadi pada usia produktif. Efek sekunder dari cedera kepala adalah gangguan fungsi kognitif berupa fungsi memori, visuospasial, perhatian dan konsentrasi, bahasa, kalkulasi, dan orientasi. Masih sedikitnya penelitian tentang penilaian fungsi memori pada pasien cedera kepala di Indonesia. Tujuan Memaparkan gambaran penurunan fungsi kognitif terutama fungsi memori pada pasien cedera kepala derajat sedang dengan edema serebri.Metode Studi deskriptif dengan desain potong-lintang menggunakan kuesioner MMSE dan MoCA-INA sebagai modalitas penilaian.Hasil Dari 30 pasien cedera kepala traumatik derajat sedang didapatkan rerata skor MMSE adalah 27.1±2.13 (interval 20-29). Rerata skor MoCA-INA adalah 24.4±2.99 (interval 16-28). Kedua skor menunjukkan bahwa MoCA-INA memiliki rerata yang lebih rendah dan rentang skor yang lebih luas. Domain yang paling banyak terganggu adalah fungsi memori recall (98%)Kesimpulan Secara keseluruhan pasien dengan cedera kepala traumatik dengan edema serebri mengalami gangguan fungsi memori terutama area memori eksplisit berupa fungsi recall. Tatalaksana kuratif dan rehabilitatif secara adekuat dan berkelanjutan diperlukan untuk mempercepat proses penyembuhanKata Kunci Cedera Kepala Traumatik Derajat Sedang, Fungsi Memori, MMSE, MoCA-INAAbstract. Background Traumatic brain injury is still a major cause of disability and death. Most occur in productive age. Secondary effects of brain injury are impaired cognitive function in the form of memory, visuospatial, attention and concentration, language, calculation, and orientation. There are few research on the assessment of memory function in brain injury patients in Indonesia.Purpose To describes the decreasing cognitive function, particularly memory function in patients with moderate brain injury with cerebral edema.Method Descriptive study with cross-sectional design using MMSE and MoCA-INA questionnaires as assessment modalities.Results Of the 30 patients with moderate-grade traumatic head injury, the mean MMSE score was 27.1 ± 2.13 (intervals 20-29). The average MoCA-INA score is 24.4 ± 2.99 (intervals 16-28). Both scores indicate that the MoCA-INA has a lower mean and a wider score range. The most disturbed domain is recall memory function (96%)Conclusion Overall patients with traumatic brain injury with cerebral edema experience impaired memory function, especially the area of explicit memory in the form of recall function. Adequate and sustainable curative and rehabilitative management is needed to accelerate the healing process Keywords Traumatic Head Injury Moderate Level, Memory Function, MMSE, MoCA-INA

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