Acute Management of Traumatic Brain Injury

Total Page:16

File Type:pdf, Size:1020Kb

Acute Management of Traumatic Brain Injury Acute Management of Traumatic Brain Injury David Chesler, MD PhD Assistant Professor of Neurological Surgery and Pediatrics Co-Director of Pediatric Neurosurgery Department of Neurological Surgery Stony Brook University School of Medicine Traumatic Brain Injury No Financial Disclosures Traumatic Brain Injury Teaching Objectives • Describe the initial physical assessment and pertinent radiographic studies to evaluating a patient suspected of having a traumatic brain injury • Describe the indications for placement of an invasive Intracranial Pressure Monitor • Discuss the medical management of acute intracranial hypertension in TBI patients • Discuss the role for surgical intervention in the management of acute TBI Traumatic Brain Injury Overview of Traumatic Brain Injury • Approximately 1.7 million people with TBI annually • Contributes to 30.5% of all injury- related deaths in the US • Around 75% of TBI are mild forms of TBI • In 2000, the annual direct and indirect cost of TBI in the US was estimated at $60 billion source: https://www.cdc.gov/traumaticbraininjury/pdf/bluebook_factsheet -a.pdf Traumatic Brain Injury Overview of Traumatic Brain Injury • Falls are leading cause of TBI with highest rates in children age 0-4 and adults > 75 • Falls account for the highest frequency of TBI-related emergency room visits • MVAs are the leading cause of TBI-related deaths; rates are highest in adults 20-24 source: https://www.cdc.gov/traumaticbraininjury/pdf/bluebook_factsheet -a.pdf Traumatic Brain Injury Vocabulary of TBI • Glasgow Coma Score • mild 13-15 • moderate 9-12 • severe 3-8 Traumatic Brain Injury Vocabulary of TBI • Types of Intracranial Injuries • Intracranial hemorrhage • subdural hematoma • epidural hematoma • intraparenchymal hematoma • diffuse axonal injury or shear injury • Fractures • open vs closed • displaced vs non-displaced Traumatic Brain Injury Vocabulary of TBI • Types of Intracranial Injuries • Intracranial hemorrhage • subdural hematoma • epidural hematoma • intraparenchymal hematoma • diffuse axonal injury or shear injury • Fractures • open vs closed • displaced vs non-displaced Traumatic Brain Injury Vocabulary of TBI • Types of Intracranial Injuries • Intracranial hemorrhage • subdural hematoma • epidural hematoma • intraparenchymal hematoma • diffuse axonal injury or shear injury • Fractures • open vs closed • displaced vs non-displaced Traumatic Brain Injury Vocabulary of TBI • Types of Intracranial Injuries • Intracranial hemorrhage • subdural hematoma • epidural hematoma • intraparenchymal hematoma • diffuse axonal injury or shear injury • Fractures • open vs closed • displaced vs non-displaced Traumatic Brain Injury Vocabulary of TBI • Types of Intracranial Injuries • Intracranial hemorrhage • subdural hematoma • epidural hematoma • intraparenchymal hematoma • diffuse axonal injury or shear injury • Fractures • open vs closed • displaced vs non-displaced Traumatic Brain Injury Vocabulary of TBI • Types of Intracranial Injuries • Intracranial hemorrhage • subdural hematoma • epidural hematoma • intraparenchymal hematoma • diffuse axonal injury or shear injury • Fractures • open vs closed • displaced vs non-displaced Traumatic Brain Injury Vocabulary of TBI • Types of Intracranial Injuries • Intracranial hemorrhage • subdural hematoma • epidural hematoma • intraparenchymal hematoma • diffuse axonal injury or shear injury • Fractures • open vs closed • displaced vs non-displaced Traumatic Brain Injury Vocabulary of TBI • Types of Intracranial Injuries • Intracranial hemorrhage • subdural hematoma • epidural hematoma • intraparenchymal hematoma • diffuse axonal injury or shear injury • Fractures • open vs closed • displaced vs non-displaced Traumatic Brain Injury Initial Assessment of TBI patient • A airway • B breathing • C circulation • Glasgow coma scale (GCS) • Neurological function • ASIA Motor Score for patients with suspected spinal cord injury able to participate • Imaging - Depends on mechanism of injury • CT brain is gold standard for initial assessment of TBI • MRI more important is assessment of CT occult imaging or prognostic evaluation • Labs • CBC, CMP, PT/INR/PTT, ARU/PRU, T&S, Tox/EtOH, Lactate, ABG Traumatic Brain Injury Management of Traumatic Brain Injury Medical Surgical • Ventilation • ICP monitoring • BP control • bolt vs ventriculostomy • Manipulate Serum Osmolarity • CSF diversion • Sedation and Analgesia • ventriculostomy vs lumbar drain • Normothermia • Seizure prophylaxis • Craniotomy/Evacuation • Correction of Coagulopathy • Decompressive Craniectomy Traumatic Brain Injury Seizure Prophylaxis • AEDs for 7 days in patients with CT positive TBI • SDH, SAH, ICH, not EDH • Dilantin (phenytoin) or Cerebryx (fosphenytoin) recommended • Keppra (levetiracetam) widely used however no data to support use over dilantin • Use of AEDs shown to reduce incidence of seizure initially following injury but has no effect on long-term risk of seizure. • If seizure in first 7 days, recommendation is for continuation of AEDs for at least three months with reassessment by neurology at that time to determine ongoing therapy. source: Carney et al. 2016. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery Traumatic Brain Injury Correction of Coagulopathy • All antiplatelet and anticogulation agents should be held and coagulopathy reversed. • Antiplatelet agents are reversed through “time” and the administration of platelets • Remember that any “onboard” agents will affect administered platelets • Coumadin • FFP, Cryoprecipitate, Activated Factor VII (NovoSeven), PCC or activated PCC (e.g. Kcentra) can all be used depending on institutional practices and individual patient considerations. • NOACs • Reversal is dependent on agent in question, most often PCC or activated PCC is recommended • Specific antidotes do exist for some (e.g. Praxabind) • Recommend involvement of hematology EARLY to facilitate appropriate reversal Traumatic Brain Injury Sedation and Analgesia • Use of sedating medications should be used with caution. • Must balance indications for sedation or analgesia with need to maintain ability to obtain neurologic examination. • Sedation is not the same as controlling blood pressure (unless hypertension is directly related to agitation) • Continuous infusion of SHORT acting medications for sedation • propofol – first line agent; check daily lactate and myoglobin to assess for development of propofol infusion syndrome • fentanyl – first line agent • versed • dexmetomidine (Precedex) - can be used in lieu of propofol in pediatric patients or in cases of PIS however not as effective for sedation or ICP control • Barbiturates are reserved for the treatment of intracranial hypertension REFRACTORY to surgical and conventional medical therapy Traumatic Brain Injury Ventilation • In patients with poor GCS, consider intubation for airway protection and respiratory support • In the absence of intracranial hypertension, normocarbia should be maintained. (PaCO2 30-40) • Hyperventilation should be avoided in the initial 24h after injury. (Can compromise cerebral blood flow) • Hyperventilation can be used as a temporizing measure in the management of intracranial hypertension. (PaCO2 maintained > 25) • Early tracheostomy can be considered for reduction in incidence of VAP if felt patient unlikely to promptly wean from mechanical ventilation (and perceived benefit outweighs risk) source: Carney et al. 2016. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery Traumatic Brain Injury Normothermia • Aggressively treat febrile state • Increased body temperature results in increased cerebral metabolism which can contribute to secondary injury • Treatment is through direct cooling, antipyretics and treating underlying cause if known (e.g. Infection) • No data to support the use of early or short-term hypothermia in the treatment of diffuse TBI source: Carney et al. 2016. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery Traumatic Brain Injury Medical Management of ICP – The Basics •Monro–Kellie Doctrine : TV = CSF + blood+ brain •Normal ICP (mmHg) • adult 0-15 (upper limit of normal is 20) • young children 3-7 • infants 0-6 •CPP = MAP – ICP • Goal CPP is ADULT ~60-70 • Goal CPP in PEDIATRIC >50-55 • CPP should not be necessarily chased by pushing MAP in patients with cerebral dysregulation source: Carney et al. 2016. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery source: http://aneskey.com/increased-intracranial-pressure-2/ Traumatic Brain Injury Hyperosmolar Therapy for Intracranial Hypertension • Works on the premise of "drawing" free water out of the brain into the intravascular compartment. • Medications are typically administered in periodic boluses • Though some centers use continuous infusions, there is no data to support this practice over bolus therapy. • Mannitol • Dosed as 0.5-1g/kg IV q6h • Dehydrates brain thereby lowering ICP but ALSO acts a diuretic which can deplete the intravascular volume which can cause HYPOTENSION. • Hypertonic Saline (HTS) • Dosed as 250-500ml of 3% NaCl, 150ml of 7.5% NaOAc or 30ml of 23.4% NaCl • Decision as to which "flavor" of HTS used based on institutional culture as well as systematic evaluation of volume status, serum pH and goal of therapy. Traumatic Brain Injury Intracranial Pressure (ICP) Monitoring • Intracranial pressure (ICP) should be monitored in all salvageable patients with a severe
Recommended publications
  • 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
    [Show full text]
  • Management of the Head Injury Patient
    Management of the Head Injury Patient William Schecter, MD Epidemilogy • 1.6 million head injury patients in the U.S. annually • 250,000 head injury hospital admissions annually • 60,000 deaths • 70-90,000 permanent disability • Estimated cost: $100 billion per year Causes of Brain Injury • Motor Vehicle Accidents • Falls • Anoxic Encephalopathy • Penetrating Trauma • Air Embolus after blast injury • Ischemia • Intracerebral hemorrhage from Htn/aneurysm • Infection • tumor Brain Injury • Primary Brain Injury • Secondary Brain Injury Primary Brain Injury • Focal Brain Injury – Skull Fracture – Epidural Hematoma – Subdural Hematoma – Subarachnoid Hemorrhage – Intracerebral Hematorma – Cerebral Contusion • Diffuse Axonal Injury Fracture at the Base of the Skull Battle’s Sign • Periorbital Hematoma • Battle’s Sign • CSF Rhinorhea • CSF Otorrhea • Hemotympanum • Possible cranial nerve palsy http://health.allrefer.com/pictures-images/ Fracture of maxillary sinus causing CSF Rhinorrhea battles-sign-behind-the-ear.html Skull Fractures Non-depressed vs Depressed Open vs Closed Linear vs Egg Shell Linear and Depressed Normal Depressed http://www.emedicine.com/med/topic2894.htm Temporal Bone Fracture http://www.vh.org/adult/provider/anatomy/ http://www.bartleby.com/107/illus510.html AnatomicVariants/Cardiovascular/Images0300/0386.html Epidural Hematoma http://www.chestjournal.org/cgi/content/full/122/2/699 http://www.bartleby.com/107/illus769.html Epidural Hematoma • Uncommon (<1% of all head injuries, 10% of post traumatic coma patients) • Located
    [Show full text]
  • 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 .
    [Show full text]
  • Intracranial Hemorrhage As Initial Presentation of Cerebral Venous Sinus Thrombosis
    Case Report Journal of Heart and Stroke Published: 31 Dec, 2019 Intracranial Hemorrhage as Initial Presentation of Cerebral Venous Sinus Thrombosis Joseph Y Chu1* and Marc Ossip2 1Department of Medicine, University of Toronto, Canada 2Department of Diagnostic Imaging, William Osler Health System, Canada Abstract Intracranial Hemorrhage (ICH) as initial presentation is an uncommon complication of Cerebral Venous-Sinus Thrombosis (CVT). Clinical and neuro-imaging studies of 4 cases of ICH due cerebral venous-sinus thrombosis seen at the William Osler Health System in Toronto will be presented. Discussion of the immediate and long-term management of these interesting cases will be reviewed with emphasis on the appropriate neuro-imaging studies. Literature review of Direct Oral Anticoagulants (DOAC) in the long-term management of these challenging cases will be discussed. Introduction The following are four cases of Cerebral Venous-Sinus Thrombosis (CVT) who present initially as Intracranial Hemorrhage (ICH). Clinical details, including immediate and long term management and neuro-imaging studies are presented. Results Case 1 A 43 years old R-handed house wife, South-Asian decent, who was admitted to hospital on 06- 10-2014 with sudden headache and right hemiparesis. Her past health shows no prior hypertension or stroke. She is not on any hormone replacement therapy, non-smoker and non-drinker. Married with 1 daughter. Examination shows BP=122/80, P=70 regular, GCS=15, with right homonymous hemianopsia, right hemiparesis: arm=leg 1/5, extensor R. Plantar response. She was started on IV Heparin after her unenhanced CT showed acute left parietal intracerebral hemorrhage and her MRV showed extensive sagittal sinus thrombosis extending into the left transverse OPEN ACCESS sinus (Figures 1,2).
    [Show full text]
  • 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.
    [Show full text]
  • A Review of Traumatic Axonal Injury
    Acta Medica 2021; 52(2): 102-108 acta medica REVIEW A Review of Traumatic Axonal Injury Dicle Karakaya1, [MD] ABSTRACT ORCID: 0000-0003-1939-6802 Traumatic brain injury is a major cause of mortality and neurological Ahmet İlkay Işıkay2, [MD] disability worldwide and varies according to its cause, pathogenesis, ORCID: 0000-0001-7790-4735 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 1Hacettepe University, Faculty of Medicine, Department disruption of axonal transport, axonal swelling, secondary axonal of Neurosurgery, Ankara, Turkey disconnection and Wallerian degeneration, respectively. However, traumatic axonal injury is difficult to define clinically, it should be Corresponding Author: Ahmet İlkay Işıkay considered in patients with Glasgow coma score < 8 for more than six Hacettepe University, Faculty of Medicine, Department hours after trauma and diffuse tensor imaging and sensitivity-weighted of Neurosurgery, Sıhhiye/Ankara, Turkey imaging MRI sequences are highly sensitive in its diagnosis. Glasgow Phone: +90 312 305 17 15 coma score at the time of presentation, location and severity of axonal E-mail: [email protected] damage are prognostic factors for clinical outcome. https://doi.org/10.32552/2021.ActaMedica.467 Keywords: Diffuse, traumatic, axonal, injury. Received: 29 May 2020, Accepted: 9 March 2021, Published online: 8 June 2021 INTRODUCTION Traumatic axonal injury (TAI) is a distinct it is not diffuse but actually widespread and/or clinicopathological topic that can cause severe multifocal [3].
    [Show full text]
  • Symptomatic Intracranial Hemorrhage (Sich) and Activase® (Alteplase) Treatment: Data from Pivotal Clinical Trials and Real-World Analyses
    Symptomatic intracranial hemorrhage (sICH) and Activase® (alteplase) treatment: Data from pivotal clinical trials and real-world analyses Indication Activase (alteplase) is indicated for the treatment of acute ischemic stroke. Exclude intracranial hemorrhage as the primary cause of stroke signs and symptoms prior to initiation of treatment. Initiate treatment as soon as possible but within 3 hours after symptom onset. Important Safety Information Contraindications Do not administer Activase to treat acute ischemic stroke in the following situations in which the risk of bleeding is greater than the potential benefit: current intracranial hemorrhage (ICH); subarachnoid hemorrhage; active internal bleeding; recent (within 3 months) intracranial or intraspinal surgery or serious head trauma; presence of intracranial conditions that may increase the risk of bleeding (e.g., some neoplasms, arteriovenous malformations, or aneurysms); bleeding diathesis; and current severe uncontrolled hypertension. Please see select Important Safety Information throughout and the attached full Prescribing Information. Data from parts 1 and 2 of the pivotal NINDS trial NINDS was a 2-part randomized trial of Activase® (alteplase) vs placebo for the treatment of acute ischemic stroke. Part 1 (n=291) assessed changes in neurological deficits 24 hours after the onset of stroke. Part 2 (n=333) assessed if treatment with Activase resulted in clinical benefit at 3 months, defined as minimal or no disability using 4 stroke assessments.1 In part 1, median baseline NIHSS score was 14 (min: 1; max: 37) for Activase- and 14 (min: 1; max: 32) for placebo-treated patients. In part 2, median baseline NIHSS score was 14 (min: 2; max: 37) for Activase- and 15 (min: 2; max: 33) for placebo-treated patients.
    [Show full text]
  • 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.
    [Show full text]
  • Canadian Stroke Best Practice Recommendations
    CANADIAN STROKE BEST PRACTICE RECOMMENDATIONS MANAGEMENT OF SPONTANEOUS INTRACEREBRAL HEMORRHAGE Seventh Edition - New Module 2020 Ashkan Shoamanesh (Co-chair), M. Patrice Lindsay, Lana A Castellucci, Anne Cayley, Mark Crowther, Kerstin de Wit, Shane W English, Sharon Hoosein, Thien Huynh, Michael Kelly, Cian J O’Kelly, Jeanne Teitelbaum, Samuel Yip, Dar Dowlatshahi, Eric E Smith, Norine Foley, Aleksandra Pikula, Anita Mountain, Gord Gubitz and Laura C. Gioia(Co-chair), on behalf of the Canadian Stroke Best Practices Advisory Committee in collaboration with the Canadian Stroke Consortium and the Canadian Hemorrhagic Stroke Trials Initiative Network (CoHESIVE). © 2020 Heart & Stroke October 2020 Heart and Stroke Foundation Management of Spontaneous Intracerebral Hemorrhage Canadian Stroke Best Practice Recommendations Table of Contents CANADIAN STROKE BEST PRACTICE RECOMMENDATIONS MANAGEMENT OF SPONTANEOUS INTRACERBRAL HEMORRHAGE SEVENTH EDITION, 2020 Table of Contents Topic Page Part One: Canadian Stroke Best Practice Recommendations Introduction and Overview I. Introduction 3 II. Spontaneous Intracerebral Hemorrhage Module Overview 3 III. Spontaneous Intracerebral Hemorrhage Definitions 4 IV. Guideline Development Methodology 4 V. Acknowledgements, Funding, Citation 6 VI. Figure One: Intracerebral Hemorrhage Patient Flow Map 8 Part Two: Canadian Stroke Best Practice Recommendations Spontaneous Intracerebral Hemorrhage 1. Emergency Management of Intracerebral Hemorrhage 9 1.1 Initial Clinical Assessment of Intracerebral Hemorrhage 9 1.2 Blood Pressure Management 10 1.3 Management of Anticoagulation 11 1.4 Consultation with Neurosurgery 12 1.5 Neuroimaging 12 1.5.1 Recommended additional urgent neuroimaging to confirm ICH diagnosis 12 1.5.2 Recommended additional etiological neuroimaging 13 1.6 Surgical management of Intracerebral Hemorrhage 13 Box One: Symptoms of Intracerebral Hemorrhage: 15 Box Two: Modified Boston Criteria (Linn 2010) 16 2.
    [Show full text]
  • Diffuse Axonal Injury in Head Trauma
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.52.7.838 on 1 July 1989. Downloaded from Journal ofNeurology, Neurosurgery, and Psychiatry 1989;52:838-841 Diffuse axonal injury in head trauma PETER C BLUMBERGS, NIGEL R JONES, JOHN B NORTH From the Neuropathology Laboratory, Institute ofMedical and Veterinary Science and Neurosurgery Department, Royal Adelaide Hospital, Adelaide, South Australia SUMMARY Diffuse axonal injury (DAI) as defined by detailed microscopic examination was found in 34 of 80 consecutive cases of head trauma surviving for a sufficient length of time to be clinically assessed by the Royal Adelaide Hospital Neurosurgery Unit. The findings indicate that there is a spectrum ofaxonal injury and that one third ofcases ofDAI recovered sufficiently to talk between the initial head injury producing coma and subsequent death. The macroscopic "marker" lesions in the corpus callosum and dorsolateral quadrants of the brainstem were present in only 15/34 of the cases and represented the most severe end of the spectrum of DAI. Diffuse axonal injury (DAI) that is, widespread superior cerebellar peduncles, (2) evidence of diffuse damage to axons in the white matter of the brain, was damage to axons. originally defined by Strich' and the concept was Patients who sustain severe DAI are unconscious expanded by Adams et al.2 Strich described diffuse from the moment ofimpact, do not experience a lucid Protected by copyright. degeneration ofthe cerebral white matter in a series of interval, and remain unconscious, vegetative
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]