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AZ ÉLETTUDOMÁNYI- KLINIKAI FELSŐOKTATÁS GYAKORLATORIENTÁLT ÉS HALLGATÓBARÁT
KORSZERŰSÍTÉSE A VIDÉKI KÉPZŐHELYEK NEMZETKÖZI VERSENYKÉPESSÉGÉNEK ERŐSÍTÉSÉRE
TÁMOP-4.1.1.C-13/1/KONV-2014-0001
Andras Buki M.D., Ph.D.,D.Sc.Department of Neurosurgery, Medical Faculty of Pecs University, Pecs, Hungary, H-7624
Identification andClassification of TBI
• epidemiology
• classification – injury
• classification – injured: triage
• no injury to the skull can be as trivial or so
severe to deny treatment
Hippocrates of Kos (460–377 BC)
MOTTO
TBI Definition VA/DoD
• VA/DoD “Clinical Practice Guideline For Management of Concussion/ Mild Traumatic
Brain Injury” (V1.0 2009) and Brain Trauma Foundation, AANS and ANC joint
“Guidelines for the management of the Severe Traumatic Brain Injury” (3rd edition,
2007) has defined traumatic brain injury as a
traumatically induced structural injury and/or physiological
disruption of brain function as a result of an external force that
is indicated by new onset or worsening of at least one of the
following clinical signs, immediately following the event:
4
TBI Definition VA/DoD II
• loss of or a decreased level of consciousness (LOC)
• loss of memory for events immediately before or after the injury
(post-traumatic amnesia [PTA])
• alteration in mental state (confusion, disorientation, slowed thinking
etc.) (Alteration of consciousness/mental state [AOC])
• Neurological deficits (weakness, loss of balance, change in vision,
praxis, paresis/plegia, sensory loss, aphasia, etc.) that may or may
not be transient
• Intracranial lesion
• A computed tomography scan (CT or CAT scan) is the gold
standard for the radiological assessment of a TBI patient.
5
• epidemiology
• classification – injury
• classification – injured: triage
Traumatic brain injury…
• …the silent epidemic
• …the disease of unmet medical need
• …leading cause of mortality in the active
population
• 2.1 million TBI cases per year causing
100,000 deaths and
500,000 hospitalizations
• TBI-related death rate of the population under 35 years of age is3.5 times as many as that of cancer and heart disease together
• 90,000 survivors will endure life-long debilitating loss of function
• 5,000 new cases of epilepsy
• 2,000 permanent vegetative state
• The cumulative societal cost per year for TBI is $48 billion
(Lewin I. C. F: Head injuries: costs and consequences. J.Head.Trauma.Rehabil. 67:76-91, 1991.)
The significance of severe TBI
TBI in the Military
• penetrating brain injuries
claim 25% of soldiers killed
in battle
• 2/3 of casualties have brain
injuries and concussion is
growing military medical
problem
http://www.brainandspinalcord.org/brain-injury/statistics.html
Mild Traumatic Brain Injury (MTBI) in Sports• 1.6 - 3.8 million sports related
concussions occur each year
• N.F.L. found that dementia-related
diseases are much higher in former
players than the national population
• Sports incidence of TBI (5-18 yrs of
age)
– Cycling: 64,993
– Football: 36,412
– Baseball and Softball: 25,079
– Basketball: 24,701
– Powered RV: 24,090
– Skateboards/Scooters w/power:
18,542
– Soccer: 17,108
– Skateboards/Scooters: 16,477
http://educationalissues.suite101.com/article.cfm/tbi_statistics
http://www.cdc.gov/NCIPC/tbi/FactSheets/Concussion_in_Sports_factsheet.pdf
September 26, 2009 Florida vs Kentucky, Tim Tebow
from Univ. of Florida suffered a mild concussion
Emerging (but debated…)
• Mild traumatic brain injury
• CT negative, MRI positive
• SWI negative, MRI positive
• Post-concussive syndrome
• PTSD
The burden of traumatic brain injury
• Traumatic brain injury is the primary cause
of death under 40
• WHO estimates that until 2020 TBI will be
the third most frequent cause of death in
the Earth(Langlois et al., J. Head Trauma Rehabil. 2006, 21, 375-378
Murray et al. Lancet 1997, 349, 1436-1442)
Intervention GBP
Se cholesterol check-up (age40-69) 220
Neurosurgical care for TBI 240
Neurosurgical care for SAH 490
Stroke prevention with anti-hypertensive medication (age40-64) 940
pm implantation 1100
Kidney transplantation 4710
Neurosurgical care for brain tumors 107780
GBP/QALY by the NHS:
• epidemiology
• classification – injury
• classification – injured: triage
PRIMARY BRAIN INJURY
SECONDARY BRAIN INJURYhypoxiahypoperfusion
ASSOCIATED CNS INJURYassociated C-spine (CO-II) injurytandem injury
ASSOCIATED INJURYassociated multiorgan injury/failure (MOF)
General classification
PRIMARY BRAIN INJURY
• occurs at the time of impact
• almost immediate clinical effects
• refractory to most treatment
• can be influenced by preventive measures
SECONDARY BRAIN INJURY
• occurs at some time after the impact
• characterized by hypoperfusion/hypoxia
• propagates gradually
• preventable and treatable
PRIMARY BRAIN INJURY
SECONDARY BRAIN INJURY
ASSOCIATED CNS INJURYassociated C-spine (CO-II) injurytandem injury
ASSOCIATED INJURYmultiple/polytraumaassociated multiorgan injury/failure (MOF)
General classification
CLOSED – PENETRATINGsimple open skull fracture depressed „compound fracture”
skull-base fracture
Classic „anatomical”: on the basis of skull injury (reflects the probability of intracranial infection)
Advanced Trauma Life Support®-ATLS ®
• circumstances of injury + energy/forces + type of impact
• potential structural damage, pathobiological processes evoked
Potential forces
• STATIC
• DYNAMIC– impact
– acceleration-deceleration
Focal Diffuse
• contusioncoup - contrecoup
• epidural hemorrhage• subdural hemorrhage
Patho-morphology
Diffuse Axonal Injury (DAI)Hypoxic Brain DamageBrain SwellingDiffuse Vascular InjuryDiffuse Neuronal Somatic Injury
IMPACT-TYPE, dynamic forcesAcceleration-deceleration-type,dynamic forces
Focal Diffuse
• contusioncoup - contrecoup
• epidural hemorrhage• subdural hemorrhage
Patho-morphology
Diffuse Axonal Injury (DAI)Hypoxic Brain DamageBrain SwellingDiffuse Vascular InjuryDiffuse Neuronal Somatic Injury
IMPACT-TYPE, dynamic forcesAcceleration-deceleration-type,dynamic forces
• epidemiology
• classification – injury
• classification – injured: triage
Triage
• pre-CT- classification
• classification upon the severity of brain injury
Classification of TBI Severity adopted
from 2009 VA/DOD Guideline
Neurosurgery. 2009 Apr;64(4):690-6; discussion 696-7. doi: 10.1227/01.NEU.0000340796.18738.F7.
Patients with moderate head injury: a prospective multicenter study of 315 patients.
Compagnone C, d'Avella D, Servadei F, Angileri FF, Brambilla G, Conti C, Cristofori L, Delfini R, Denaro L, Ducati A, Gaini SM,
Stefini R, Tomei G, Tagliaferri F, Trincia G, Tomasello F.
• Moderate head injury: GCS 9-12 is NOT a homogenious group
• Neuroworsening, seizures, and medical complications as outcome predictors with a GCS of 11 to 13
• Low motor GCS score ismore outcome-related in patients with GCS of 9 and 10.
Saatman KE, Duhaime AC, Bullock R, Maas AI, Valadka A, Manley GT; Workshop Scientific Team and Advisory Panel Members. Classification of traumatic brain injury for targeted therapies. J Neurotrauma. 2008;25(7):719-38.
• Current classifications of TBI are outdated
• Classifications that describe the whole injury spectrum are needed
Triage
• Probability of intracranial hemorrhage following traumatic brain injury:
LOW:
lack of factors indicating medium and high probability
patients are discharged with warning notices
• Probability of intracranial hemorrhage following traumatic brain injury:
Medium:
1., LOC2., Progressive headache3., Alcohol/drug intoxication4., Seizure 5., Unreliable history6., Age under 2y7., Repeated vomiting8., Amnesia9., Physical signs of skull fracture10.,Repeated trauma11.,Severe maxillo-facial trauma12.,Child abuse13.,Significant subgaleal swelling/collection14.,Coagulopathy15.,Diabetes
CT scan followed by discharge or observation
diagnostic measures:
• ultrasound
• transillumination
• CT
• MRI
• X-Ray NOOOOOOO!!!!!!!!
• Probability of intracranial hemorrhage following traumatic brain injury:
HIGH:
1., GCS 12 or less2., Focal neurological signs3., Decrease in GCS value4., Open/penetrating skull injury5., On the basis of injury-mechanism intracranial injury is suspected.
Immediate transfer to a neurosurgical department
Head injured patients (outpatient/emergency)
room)
Low risk
- initial GCS over 14
- from “medium risk”-categories only the
following:
- sober responsible adult supervision - immediate access to transportation
- repeated injury can be excluded
informed discharge with
warning notices
All other cases:
observation on the floor
Medium risk
Observation on the floor/CT
Normal CT
risk Pathological CT
Consult a neurosurgeon
Deterioration amnesia
loss of consciousness
No deterioration
• Adverse outcome of an intracranial hematoma is so costly that it more than balances the expense of CT scans.
• In cost-effectiveness models the liberal use of CT scanning in mild TBI appears justified.
• Stein SC J Trauma. 2007 May;62(5):1309.
• Geijerstam et al. Emerg Med J. 2004 Jan;21(1):54-8.
Undén J, Ingebrigtsen T, Romner B; Scandinavian Neurotrauma Committee (SNC) Scandinavian guidelines for
initial management of minimal, mild and moderate head injuries in adults: an evidence and consensus-based
update. BMC Med. 2013 Feb 25;11:50.
J Neurotrauma. 2013 Mar 14. [Epub ahead of print]
GFAP-BDP as an Acute Diagnostic Marker in Traumatic Brain Injury: Results from the
prospective TRACK-TBI Study.
Okonkwo DO, Yue JK, Puccio AM, Panczykowski D, Inoue T, McMahon PJ, Sorani MD, Yuh EL,
Lingsma H, Maas A, Valadka A, Manley GT M D Ph D.
Source
University of Pittsburgh, Dept of Neurological Surgery, Pittsburgh, Pennsylvania, United States;
Abstract
Reliable diagnosis of traumatic brain injury (TBI) is a major public health need. Glial fibrillary acidic
protein (GFAP) is expressed in the central nervous system and breakdown products (GFAP-BDP) are
released following parenchymal brain injury. Here we evaluate the diagnostic accuracy of elevated
levels of plasma GFAP-BDP in TBI. Participants were identified as part of the prospective
Transforming Research And Clinical Knowledge in Traumatic Brain Injury (TRACK-TBI) Study. Acute
plasma samples (<24 hours) were collected from patients presenting with head injury who had CT
imaging. The ability of GFAP-BDP level to discriminate patients with demonstrable traumatic lesions
on CT and with failure to return to pre-injury baseline at 6 months was evaluated by the area under the
receiver operating characteristic curve (AUC). Of the 215 patients included for analysis, 83% suffered
mild, 4% moderate, and 13% severe TBI; 54% had acute traumatic lesions on CT. The ability of
GFAP-BDP level to discriminate patients with traumatic lesions on CT as evaluated by AUC was 0.88
(95%CI, 0.84-0.93). The optimal cutoff of 0.68ng/ml for plasma GFAP-BDP level was associated with
a 21.61 Odds Ratio for traumatic findings on head CT. Discriminatory ability of unfavorable 6-month
outcome was lower, AUC 0.65 (95% CI, 0.55-0.74), with a 2.07 Odds Ratio. GFAP-BDP levels reliably
distinguish the presence and severity of CT scan findings in TBI patients. While these findings confirm
and extend prior studies, a larger prospective trial is still needed to validate the use of GFAP-BDP as a
routine diagnostic biomarker for patient care and clinical research. (ClinicalTrials.gov number
NCT01565551;NIH Grant 1RC2NS069409).
Summary
• Current characterization of TBI is outdated
• Emphasise should be on timely recognition of patients at risk
• Novel classification/characterization is needed to describe the entire injury-spectrum
Childhood:1 no response2 unrecognizable voices (sounds but no crying)3 unproper words (crying)4 non comprehensive talk (agitated)5 oriented (smiles, follows objects, finger)
•DEFINITIONS AND CLASSIFICATION
•SYMPTOMS AND SIGNS OF RAISED ICP
•PRIMARY ASSESSMENT OF THE HEAD INJURED
/PRIMARY ASSESSMENT IN LOC
•GENERAL PRINCIPLES OF THE TREATMENT OF THESEVERELY HEAD INJURED
•EPIDEMIOLOGY OF TRAUMATIC BRAIN INJURY
• ☺** Poor outcome under systolic
pressure of:
• 65 Hgmm 0-1 y;
• <75 Hgmm 2-5 y;
• <80 Hgmm 6-12 y;
• <90 Hgmm 13-16 y.
60
60
60
Thank You!