Guidelines for BLS/ALS Medical Providers Current As of March 2019
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Spinal Cord Injury and Traumatic Brain Injury Research Grant Program Report 2020
This document is made available electronically by the Minnesota Legislative Reference Library as part of an ongoing digital archiving project. http://www.leg.state.mn.us/lrl/lrl.asp Spinal Cord Injury and Traumatic Brain Injury Research Grant Program Report January 15, 2020 Author About the Minnesota Office of Higher Education Alaina DeSalvo The Minnesota Office of Higher Education is a Competitive Grants Administrator cabinet-level state agency providing students with Tel: 651-259-3988 financial aid programs and information to help [email protected] them gain access to postsecondary education. The agency also serves as the state’s clearinghouse for data, research and analysis on postsecondary enrollment, financial aid, finance and trends. The Minnesota State Grant Program is the largest financial aid program administered by the Office of Higher Education, awarding up to $207 million in need-based grants to Minnesota residents attending eligible colleges, universities and career schools in Minnesota. The agency oversees other state scholarship programs, tuition reciprocity programs, a student loan program, Minnesota’s 529 College Savings Plan, licensing and early college awareness programs for youth. Minnesota Office of Higher Education 1450 Energy Park Drive, Suite 350 Saint Paul, MN 55108-5227 Tel: 651.642.0567 or 800.657.3866 TTY Relay: 800.627.3529 Fax: 651.642.0675 Email: [email protected] Table of Contents Introduction 1 Spinal Cord Injury and Traumatic Brain Injury Advisory Council 1 FY 2020 Proposal Solicitation Schedule -
Neurological and Neurourological Complications of Electrical Injuries
REVIEW ARTICLE Neurologia i Neurochirurgia Polska Polish Journal of Neurology and Neurosurgery 2021, Volume 55, no. 1, pages: 12–23 DOI: 10.5603/PJNNS.a2020.0076 Copyright © 2021 Polish Neurological Society ISSN 0028–3843 Neurological and neurourological complications of electrical injuries Konstantina G. Yiannopoulou1, Georgios I. Papagiannis2, 3, Athanasios I. Triantafyllou2, 3, Panayiotis Koulouvaris3, Aikaterini I. Anastasiou4, Konstantinos Kontoangelos5, Ioannis P. Anastasiou6 1Neurological Department, Henry Dunant Hospital Centre, Athens, Greece 2Orthopaedic Research and Education Centre “P.N. Soukakos”, Biomechanics and Gait Analysis Laboratory “Sylvia Ioannou”, “Attikon” University Hospital, Athens, Greece 31st Department of Orthopaedic Surgery, Medical School, National and Kapodistrian University of Athens, Athens, Greece 4Medical School of Athens, National and Kapodistrian University of Athens, Athens, Greece 51st Department of Psychiatry, National and Kapodistrian University of Athens, Eginition Hospital, Athens, Greece 61st Urology Department, Laiko Hospital, National and Kapodistrian University of Athens, Athens, Greece ABSTRACT Electrical injury can affect any system and organ. Central nervous system (CNS) complications are especially well recognised, causing an increased risk of morbidity, while peripheral nervous system (PNS) complications, neurourological and cognitive and psychological abnormalities are less predictable after electrical injuries. PubMed was searched for English language clinical observational, retrospective, -
Traumatic Brain Injury
REPORT TO CONGRESS Traumatic Brain Injury In the United States: Epidemiology and Rehabilitation Submitted by the Centers for Disease Control and Prevention National Center for Injury Prevention and Control Division of Unintentional Injury Prevention The Report to Congress on Traumatic Brain Injury in the United States: Epidemiology and Rehabilitation is a publication of the Centers for Disease Control and Prevention (CDC), in collaboration with the National Institutes of Health (NIH). Centers for Disease Control and Prevention National Center for Injury Prevention and Control Thomas R. Frieden, MD, MPH Director, Centers for Disease Control and Prevention Debra Houry, MD, MPH Director, National Center for Injury Prevention and Control Grant Baldwin, PhD, MPH Director, Division of Unintentional Injury Prevention The inclusion of individuals, programs, or organizations in this report does not constitute endorsement by the Federal government of the United States or the Department of Health and Human Services (DHHS). Suggested Citation: Centers for Disease Control and Prevention. (2015). Report to Congress on Traumatic Brain Injury in the United States: Epidemiology and Rehabilitation. National Center for Injury Prevention and Control; Division of Unintentional Injury Prevention. Atlanta, GA. Executive Summary . 1 Introduction. 2 Classification . 2 Public Health Impact . 2 TBI Health Effects . 3 Effectiveness of TBI Outcome Measures . 3 Contents Factors Influencing Outcomes . 4 Effectiveness of TBI Rehabilitation . 4 Cognitive Rehabilitation . 5 Physical Rehabilitation . 5 Recommendations . 6 Conclusion . 9 Background . 11 Introduction . 12 Purpose . 12 Method . 13 Section I: Epidemiology and Consequences of TBI in the United States . 15 Definition of TBI . 15 Characteristics of TBI . 16 Injury Severity Classification of TBI . 17 Health and Other Effects of TBI . -
Case Report Myelopathy and Amnesia Following Accidental Electrical Injury
Spinal Cord (2002) 40, 253 ± 255 ã 2002 International Spinal Cord Society All rights reserved 1362 ± 4393/02 $25.00 www.nature.com/sc Case Report Myelopathy and amnesia following accidental electrical injury J Kalita*,1, M Jose1 and UK Misra1 1Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences Lucknow, India Objective: Documentation of MRI and neurophysiological changes following accidental electrical injury. Setting: Tertiary care referral teaching hospital at Lucknow, India. Results: A 30-year-old lady developed amnesia and spastic paraparesis with loss of pin prick sensation below the second thoracic spinal segment following electrocution. Her spinal MRI was normal and cranial MRI revealed T2 hyperintensity in the right putamen. Peroneal, sural and electromyography were normal. Tibial central sensory conduction time was normal but central motor conduction time to lower limbs and right upper limb was prolonged. Conclusion: Neurophysiological study and MRI may help in understanding the pathophy- siological basis of neurological sequelae following electrical injury. Spinal Cord (2002) 40, 253 ± 255. DOI: 10.1038/sj/sc/3101275 Keywords: electrical injury; MRI; evoked potential; myelopathy; amnesia Introduction Rural electri®cation has received great attention from across the road. Her hands were wet, the road was the government for improving agricultural and small ¯ooded with water and the wire was conducting AC of scale industry development in India. This has inherent 11 000 V. Immediately, she had fallen down and the hazards because of the ignorance of villagers and poor wire stuck to her chest. The current ¯ow was maintenance of electrical cables. This results in several discontinued after about 5 min and she was discovered electrical accidents caused by the touching of live wires. -
Early Management of Retained Hemothorax in Blunt Head and Chest Trauma
World J Surg https://doi.org/10.1007/s00268-017-4420-x ORIGINAL SCIENTIFIC REPORT Early Management of Retained Hemothorax in Blunt Head and Chest Trauma 1,2 1,8 1,7 1 Fong-Dee Huang • Wen-Bin Yeh • Sheng-Shih Chen • Yuan-Yuarn Liu • 1 1,3,6 4,5 I-Yin Lu • Yi-Pin Chou • Tzu-Chin Wu Ó The Author(s) 2018. This article is an open access publication Abstract Background Major blunt chest injury usually leads to the development of retained hemothorax and pneumothorax, and needs further intervention. However, since blunt chest injury may be combined with blunt head injury that typically requires patient observation for 3–4 days, other critical surgical interventions may be delayed. The purpose of this study is to analyze the outcomes of head injury patients who received early, versus delayed thoracic surgeries. Materials and methods From May 2005 to February 2012, 61 patients with major blunt injuries to the chest and head were prospectively enrolled. These patients had an intracranial hemorrhage without indications of craniotomy. All the patients received video-assisted thoracoscopic surgery (VATS) due to retained hemothorax or pneumothorax. Patients were divided into two groups according to the time from trauma to operation, this being within 4 days for Group 1 and more than 4 days for Group 2. The clinical outcomes included hospital length of stay (LOS), intensive care unit (ICU) LOS, infection rates, and the time period of ventilator use and chest tube intubation. Result All demographics, including age, gender, and trauma severity between the two groups showed no statistical differences. -
NIH Public Access Author Manuscript J Neuropathol Exp Neurol
NIH Public Access Author Manuscript J Neuropathol Exp Neurol. Author manuscript; available in PMC 2010 September 24. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: J Neuropathol Exp Neurol. 2009 July ; 68(7): 709±735. doi:10.1097/NEN.0b013e3181a9d503. Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy following Repetitive Head Injury Ann C. McKee, MD1,2,3,4, Robert C. Cantu, MD3,5,6,7, Christopher J. Nowinski, AB3,5, E. Tessa Hedley-Whyte, MD8, Brandon E. Gavett, PhD1, Andrew E. Budson, MD1,4, Veronica E. Santini, MD1, Hyo-Soon Lee, MD1, Caroline A. Kubilus1,3, and Robert A. Stern, PhD1,3 1 Department of Neurology, Boston University School of Medicine, Boston, Massachusetts 2 Department of Pathology, Boston University School of Medicine, Boston, Massachusetts 3 Center for the Study of Traumatic Encephalopathy, Boston University School of Medicine, Boston, Massachusetts 4 Geriatric Research Education Clinical Center, Bedford Veterans Administration Medical Center, Bedford, Massachusetts 5 Sports Legacy Institute, Waltham, MA 6 Department of Neurosurgery, Boston University School of Medicine, Boston, Massachusetts 7 Department of Neurosurgery, Emerson Hospital, Concord, MA 8 CS Kubik Laboratory for Neuropathology, Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts Abstract Since the 1920s, it has been known that the repetitive brain trauma associated with boxing may produce a progressive neurological deterioration, originally termed “dementia pugilistica” and more recently, chronic traumatic encephalopathy (CTE). We review the 47 cases of neuropathologically verified CTE recorded in the literature and document the detailed findings of CTE in 3 professional athletes: one football player and 2 boxers. -
Traumatic Brain Injury(Tbi)
TRAUMATIC BRAIN INJURY(TBI) B.K NANDA, LECTURER(PHYSIOTHERAPY) S. K. HALDAR, SR. OCCUPATIONAL THERAPIST CUM JR. LECTURER What is Traumatic Brain injury? Traumatic brain injury is defined as damage to the brain resulting from external mechanical force, such as rapid acceleration or deceleration impact, blast waves, or penetration by a projectile, leading to temporary or permanent impairment of brain function. Traumatic brain injury (TBI) has a dramatic impact on the health of the nation: it accounts for 15–20% of deaths in people aged 5–35 yr old, and is responsible for 1% of all adult deaths. TBI is a major cause of death and disability worldwide, especially in children and young adults. Males sustain traumatic brain injuries more frequently than do females. Approximately 1.4 million people in the UK suffer a head injury every year, resulting in nearly 150 000 hospital admissions per year. Of these, approximately 3500 patients require admission to ICU. The overall mortality in severe TBI, defined as a post-resuscitation Glasgow Coma Score (GCS) ≤8, is 23%. In addition to the high mortality, approximately 60% of survivors have significant ongoing deficits including cognitive competency, major activity, and leisure and recreation. This has a severe financial, emotional, and social impact on survivors left with lifelong disability and on their families. It is well established that the major determinant of outcome from TBI is the severity of the primary injury, which is irreversible. However, secondary injury, primarily cerebral ischaemia, occurring in the post-injury phase, may be due to intracranial hypertension, systemic hypotension, hypoxia, hyperpyrexia, hypocapnia and hypoglycaemia, all of which have been shown to independently worsen survival after TBI. -
Mild Traumatic Brain Injury and Concussion: Information for Adults
Mild Traumatic Brain Injury and Concussion: Information for Adults Discharge Instructions You were seen today for a mild traumatic brain injury (mild TBI) or concussion. Watch for Danger Signs Use this handout to help you watch In rare cases, a dangerous blood clot that for changes in how you are feeling crowds the brain against the skull can develop or acting and to help you feel better. after a TBI. The people checking on you should call 911 or take you to an emergency Be sure to let a family member or department right away if you have: friend know about your injury and the types of symptoms to look out • A headache that gets worse and does not for. They may notice symptoms go away before you do and can help you. • Significant nausea or repeated vomiting • Unusual behavior, increased confusion, Schedule a follow-up appointment restlessness, or agitation with your regular doctor. • Drowsiness or inability to wake up Due to your injury, you may need to take some • Slurred speech, weakness, numbness, or time off from things like work or school. If so, ask decreased coordination your doctor for written instructions about when • Convulsions or seizures (shaking or you can safely return to work, school, sports, twitching) or other activities such as driving a car, riding a • Loss of consciousness (passing out) bike, or operating heavy equipment. More information on mild TBI and concussion, as well as tips to help you feel better, can be found at www.cdc.gov/TraumaticBrainInjury. Learn About Your Injury Mild TBI and concussions are brain injuries. -
Instructor Guide for Tactical Field Care 3C Communication, Evacuation Prioroties and Cpr 180801 1
INSTRUCTOR GUIDE FOR TACTICAL FIELD CARE 3C COMMUNICATION, EVACUATION PRIOROTIES AND CPR 180801 1 Tactical Combat Casualty Care for Medical Personnel August 2017 Next, we will discuss communication, evacuation priorities, and 1. (Based on TCCC-MP Guidelines 170131) CPR in TFC. Tactical Field Care 3c Communication, Evacuation Priorities and CPR Disclaimer “The opinions or assertions contained herein are the private views of the authors and are not to be construed 2. as official or as reflecting the views of the Departments Read the text. of the Army, Air Force, Navy or the Department of Defense.” - There are no conflict of interest disclosures. LEARNING OBJECTIVES Terminal Learning Objective • Communicate combat casualty care items effectively in Tactical Field Care. Enabling Learning Objectives 3. Read the text. • Identify the importance and techniques of communication with a casualty in Tactical Field Care. • Identify the importance and techniques of communicating casualty information with unit tactical leadership. INSTRUCTOR GUIDE FOR TACTICAL FIELD CARE 3C COMMUNICATION, EVACUATION PRIOROTIES AND CPR 180801 2 LEARNING OBJECTIVES Enabling Learning Objectives • Identify the importance and techniques of communicating casualty information with evacuation assets or receiving facilities. 4. Read the text. • Identify the relevant tactical and casualty data involved in communicating casualty information. • Identify the evacuation urgencies recommended in the TCCC TACEVAC “Nine Rules of Thumb” and the JTS evacuation guidelines • Identify the information requirements and format of the 9-Line MEDEVAC Request. LEARNING OBJECTIVES Terminal Learning Objective • Describe cardiopulmonary resuscitation (CPR) considerations in Tactical Field Care. Enabling Learning Objectives 5. Read the text. • Identify considerations for cardiopulmonary resuscitation in tactical field care. -
CDC Concussion Definition and Pathophysiology
Concussion Definition and Pathophysiology The Evolving Definition of Concussion CDC Physicians Toolkit; Collins, Gioia et al 2006 Regarding Cerebral Concussion…… A concussion (or mild traumatic brain injury) is a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces secondary to direct or indirect forces to the head. Disturbance of brain function is related to neurometabolic dysfunction, rather than structural brain injury, and is typically associated with normal structural imaging findings (CT Scan, MRI). Concussion may or may not involve a loss of consciousness. Concussion results in a constellation of physical, cognitive, emotional, and sleep‐related symptoms. Recovery is a sequential process and symptoms may last from several minutes to days, weeks, months, or even longer in some cases.” . Following a concussion, there are metabolic chemical changes that take place in the brain. Brain injury can occur even if there is NO loss of consciousness. More than 90% of concussions DO NOT involve loss of consciousness. Memories of events BEFORE and AFTER the concussion are MORE accurate assessments of SEVERITY than loss of consciousness. Pathophysiology of Concussions – Dr. Micky Collins, Director UPMC Sports Medicine Concussion Program Neurometabolic Cascade of Concussion During activities a concussion can occur with any type of external force to the head. These events can cause the brain to accelerate and decelerate with translational, rotational and/or angular forces. Brain injuries can result on the side of the force, cu, or the opposite side of the force, contra cu. So what exactly do these forces do to the brain? Researchers believe it leads to a wave of energy that passes through the brain tissue triggering neuronal dysfunction. -
Early Post-Traumatic Pulmonary-Embolism in Patients Requiring ICU Admission: More Complicated Than We Think!
3854 Editorial Early post-traumatic pulmonary-embolism in patients requiring ICU admission: more complicated than we think! Mabrouk Bahloul1, Mariem Dlela1, Nadia Khlaf Bouaziz2, Olfa Turki1, Hedi Chelly1, Mounir Bouaziz1 1Department of Intensive Care, Habib Bourguiba University Hospital, Sfax, Tunisia; 2Centre Intermédiaire, Rte El MATAR Km 4, Sfax, Tunisia Correspondence to: Professor Mabrouk Bahloul. Department of Intensive Care, Habib Bourguiba University Hospital, 3029 Sfax, Tunisia. Email: [email protected]. Submitted Jun 10, 2018. Accepted for publication Sep 12, 2018. doi: 10.21037/jtd.2018.09.49 View this article at: http://dx.doi.org/10.21037/jtd.2018.09.49 We read with interest the article entitled “Prevalence and traumatic thromboembolism in patients who are requiring main determinants of early post-traumatic thromboembolism an ICU admission. Nevertheless, this study as mentioned in patients requiring ICU admission” (1). In this retrospective by the authors suffers from many limitations. In fact, the study, Kazemi Darabadi et al. (1) had included to their small sample size, and also the retrospective design of database, the records of 240 trauma-patients requiring the study lead to an increased probability of some bias ICU admission, with a confirmed diagnosis of pulmonary when collecting data. In fact, in this study (1), PE was embolism (PE). The patients were categorized as subjects not screened on a daily basis. As a consequence, the late with an early PE (≤3 days) and those with a late PE (>3 days). stage PE may only be a delayed diagnosis. For instance, According to their analysis, 48.5% of the patients suffering a patient who develops with PE on day 2 but without any from PE had developed this complication within 72 h symptom(s); then he is accidentally diagnosed with PE on following a trauma event and/or after ICU admission. -
The Fund at a Glance
CytoSorbentsTM Trauma and Crush Injury TRAUMA AND CRUSH INJURIES ARE CURRENTLY LEADING CAUSES OF DEATH. Trauma and crush injuries occur frequently and from multiple sources. For example, automobile or motorcycle accidents, natural disasters, and acts of criminal violence or terrorism can all yield mild to severe trauma and crush injuries. The breadth of life-threatening conditions from trauma-induced injuries, such as lung and bowel rupture, closed head injury, crush injury and rhabdomyolysis, traumatic fractures, penetrating wound injury, and limb loss, creates a very challenging environment for clinicians to employ effective treatment strategies. Better therapies are needed to reduce the mortality in patients with severe trauma injury, reduce the risk of organ failure, reduce complications (e.g. rhabdomyolysis and infection), and decrease hospital stay length. CYTOKINE STORM AND RHABDOMYOLYSIS IN TRAUMA CAN CAUSE ORGAN FAILURE AND DEATH Trauma is a well-known trigger of the immune response, and can result in the massive, uncontrolled production of cytokines, or “cytokine storm.” Cytokines are small proteins that normally help stimulate and regulate the immune system to fight infection or injury. However, in trauma, cytokine storm can be toxic, leading to a massive systemic inflammatory response syndrome (SIRS) and a cascade of events that can kill cells and damage organs, leading to organ failure and often death. Cytokine storm exacerbates physical trauma in many ways. For example, trauma can cause: Hemorrhagic shock due to blood loss while cytokine storm causes capillary leak and intravascular volume loss, and the induction of nitric oxide that can lead to myocardial depression and peripheral vasodilation, all of which exacerbate shock Severe limb injuries that often require a tourniquet.