Traumatic Epidural and Subdural Hematoma: Epidemiology, Outcome, and Dating
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Diagnoses to Include in the Problem List Whenever Applicable
Diagnoses to include in the problem list whenever applicable Tips: 1. Always say acute or open when applicable 2. Always relate to the original trauma 3. Always include acid-base abnormalities, AKI due to ATN, sodium/osmolality abnormalities 4. Address in the plan of your note 5. Do NOT say possible, potential, likely… Coders can only use a real diagnosis. Make a real diagnosis. Neurological/Psych: Head: 1. Skull fracture of vault – open vs closed 2. Basilar skull fracture 3. Facial fractures 4. Nerve injury____________ 5. LOC – include duration (max duration needed is >24 hrs) and whether they returned to neurological baseline 6. Concussion with or without return to baseline consciousness 7. DAI/severe concussion with or without return to baseline consciousness 8. Type of traumatic brain injury (hemorrhages and contusions) – include size a. Tiny = <0.6 cm b. Small/moderate = 0.6-1 cm c. Large/extensive = >1 cm 9. Cerebral contusion/hemorrhage 10. Cerebral edema 11. Brainstem compression 12. Anoxic brain injury 13. Seizures 14. Brain death Spine: 1. Cervical spine fracture with (complete or incomplete) or without cord injury 2. Thoracic spine fracture with (complete or incomplete) or without cord injury 3. Lumbar spine fracture with (complete or incomplete) or without cord injury 4. Cord syndromes: central, anterior, or Brown-Sequard 5. Paraplegia or quadriplegia (any deficit in the upper extremity is consistent with quadriplegia) Cardiovascular: 1. Acute systolic heart failure 40 2. Acute diastolic heart failure 3. Chronic systolic heart failure 4. Chronic diastolic heart failure 5. Combined heart failure 6. Cardiac injury or vascular injuries 7. -
Two Types of Delayed Post-Traumatic Intracerebral Hematoma
Two Types of Delayed Post-Traumatic Intracerebral Hematoma Takashi TSUBOKAWA Department of Neurological Surgery, Nihon University School of Medicine, Tokyo 173 Summary The findings of repeated CT scans, clinicalcourses and pathologicalstudies in 28 cases of delayed post-traumatic intracerebral hematoma were studied retrospectivelyto elucidate the mechanism of bleeding and to establish adequate treatment. Based on the results obtained, it became clear that there are two types of delayed hematoma. In 10 of the 28 cases, initial CT findings within 6 hours after head injury revealed cerebral contusion or hemorrhagic contusion, and spots of high density scattered in the low density zone gradually became confluent to form an irregularly shaped hematoma according to follow-up CT findings. This was termed "hematoma within a contusional area." In 15 of the 28 cases, initial CT findings within 6 hours after head injury revealed no abnormal density within the brain and the hematoma appeared suddenly 3 6 days after the injury. In eight of the 15 cases, emergency surgery was performed for the removal of epidural or subdural hematoma. This type of hematoma is termed "contusional hem atoma" and constitutes the second group. In three of the 28 cases, both types of hematoma were observed. Based on histological findings for the two types of delayed hematoma. The first group may be induced by an anoxic vasodilation mechanism (Evans et al.9)), while the second group may be derived from a different mechanism related to ishemic changes and the free radical reaction caused by the reflow phenomenon (Tsubokawa et al.14-16)1 It is important to establish correct diagnoses 1for delayed hematomas based on differences between follow-up findings of repeated CT and an initial CT performed within 6 hours after head injury since the operative indications and operative results for the two groups are different as indicated by our 28 cases. -
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 -
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). -
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. -
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]. -
Sports-Related Concussions: Diagnosis, Complications, and Current Management Strategies
NEUROSURGICAL FOCUS Neurosurg Focus 40 (4):E5, 2016 Sports-related concussions: diagnosis, complications, and current management strategies Jonathan G. Hobbs, MD,1 Jacob S. Young, BS,1 and Julian E. Bailes, MD2 1Department of Surgery, Section of Neurosurgery, The University of Chicago Pritzker School of Medicine, Chicago; and 2Department of Neurosurgery, NorthShore University HealthSystem, The University of Chicago Pritzker School of Medicine, Evanston, Illinois Sports-related concussions (SRCs) are traumatic events that affect up to 3.8 million athletes per year. The initial diag- nosis and management is often instituted on the field of play by coaches, athletic trainers, and team physicians. SRCs are usually transient episodes of neurological dysfunction following a traumatic impact, with most symptoms resolving in 7–10 days; however, a small percentage of patients will suffer protracted symptoms for years after the event and may develop chronic neurodegenerative disease. Rarely, SRCs are associated with complications, such as skull fractures, epidural or subdural hematomas, and edema requiring neurosurgical evaluation. Current standards of care are based on a paradigm of rest and gradual return to play, with decisions driven by subjective and objective information gleaned from a detailed history and physical examination. Advanced imaging techniques such as functional MRI, and detailed understanding of the complex pathophysiological process underlying SRCs and how they affect the athletes acutely and long-term, may change the way physicians treat athletes who suffer a concussion. It is hoped that these advances will allow a more accurate assessment of when an athlete is truly safe to return to play, decreasing the risk of secondary impact injuries, and provide avenues for therapeutic strategies targeting the complex biochemical cascade that results from a traumatic injury to the brain. -
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. -
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. -
Selection of Treatment for Large Non-Traumatic Subdural Hematoma Developed During Hemodialysis
Korean J Crit Care Med 2014 May 29(2):114-118 / http://dx.doi.org/10.4266/kjccm.2014.29.2.114 ■ Case Report ■ pISSN: 1229-4802ㆍeISSN: 2234-3261 Selection of Treatment for Large Non-Traumatic Subdural Hematoma Developed during Hemodialysis Chul-Hee Lee, M.D., Ph.D. Department of Neurosurgery, Gyeongsang National University School of Medicine, Jinju, Korea A 49-year-old man with end-stage renal disease was admitted to the hospital with a severe headache and vomiting. On neurological examination the Glasgow Coma Scale (GCS) score was 15 and his brain CT showed acute subdural hematoma over the right cerebral convexity with approximately 11-mm thickness and 9-mm midline shift. We chose a conservative treatment of scheduled neurological examination, anticonvulsant medication, serial brain CT scanning, and scheduled hemodialysis (three times per week) without using heparin. Ten days after admission, he complained of severe headache and a brain CT showed an increased amount of hemorrhage and midline shift. Emergency burr hole trephination and removal of the hematoma were performed, after which symptoms improved. However, nine days after the operation a sudden onset of general tonic-clonic seizure developed and a brain CT demonstrated an in- creased amount of subdural hematoma. Under the impression of persistent increased intracranial pressure, the patient was transferred to the intensive care unit (ICU) in order to control intracranial pressure. Management at the ICU consisted of regular intravenous mannitol infusion assisted with continuous renal replacement therapy. He stayed in the ICU for four days. Twenty days after the operation he was discharged without specific neurological deficits. -
Article-P227.Pdf
CLINICAL ARTICLE J Neurosurg Pediatr 23:227–235, 2019 North American survey on the post-neuroimaging management of children with mild head injuries Jacob K. Greenberg, MD, MSCI,1 Donna B. Jeffe, PhD,2 Christopher R. Carpenter, MD, MSc,3 Yan Yan, MD, PhD,4 Jose A. Pineda, MD,5,6 Angela Lumba-Brown, MD,7 Martin S. Keller, MD,4 Daniel Berger, BA,1 Robert J. Bollo, MD, MS,8 Vijay M. Ravindra, MD, MSPH,8 Robert P. Naftel, MD,9 Michael C. Dewan, MD, MSCI,9 Manish N. Shah, MD,10 Erin C. Burns, MD,11 Brent R. O’Neill, MD,12 Todd C. Hankinson, MD,12 William E. Whitehead, MD, MPH,13 P. David Adelson, MD,14 Mandeep S. Tamber, MD, PhD,15 Patrick J. McDonald, MD, MHSc,16 Edward S. Ahn, MD,17 William Titsworth, MD,17 Alina N. West, MD, PhD,18 Ross C. Brownson, PhD,4,19,20 and David D. Limbrick Jr., MD, PhD1 Departments of 1Neurological Surgery, 2Medicine, 4Surgery, 5Pediatrics, and 6Neurology, 3Division of Emergency Medicine, 19Alvin J. Siteman Cancer Center, and 20Prevention Research Center, Washington University School of Medicine in St. Louis, Missouri; 7Department of Emergency Medicine, Stanford University, Stanford, California; 8Department of Neurosurgery, University of Utah School of Medicine, Salt Lake City, Utah; 9Department of Neurological Surgery, Vanderbilt University Medical Center, Nashville, Tennessee; 10Department of Neurosurgery, McGovern Medical School at University of Texas Health Science Center at Houston, Houston, Texas; 11Department of Pediatrics, Oregon Health & Science University, Portland, Oregon; 12Department of Neurosurgery, -
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