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Traumatic Brain Injury (TBI) Brain Trauma • The skull provides the brain with a protective thick, bony encasement •yet its irregular interior presents opportunities for damage to the fragile tissues it has evolved to protect Majda M Thurnher Glasgow Coma Scale Classification of TBI The Glasgow Coma Scale is based on a 15 point scale for estimating and categorizing the outcomes of brain injury on the basis of overall social capability or dependence on others. Mild (13-15): • Mechanism: closed or penetrating Moderate Disability (9-12): Loss of consciousness greater than 30 minutes • Severity: mild, moderate, severe Physical or cognitive impairments which may resolve Severe Disability (3-8): • Pathology: primary or secondary Coma: unconscious state. No meaningful response, no voluntary activities • Morphology: focal or diffuse Vegetative State (Less Than 3): Sleep wake cycles Arousal, but no interaction with environment No localized response to pain Classification of TBI Primary brain injury refers to the sudden and profound injury to the brain that is considered to 1. PRIMARY HEAD INJURY be more or less complete at the time of impact. Scalp injuries Skull fractures Extra-axial hemorrhages Intra-axial injuries Secondary brain injury refers to the changes that 2. SECONDARY HEAD INJURY evolve over a period of time (from hours to days) after Ischemia the primary brain injury. Hypoxia It includes an entire cascade of cellular, chemical, tissue, or Hypotension blood vessel changes in the brain that contribute to further Cerebral edema destruction of brain tissue. Meningitis / Abscess Increased intracranial pressure Extra-axial hemorrhages 1. PRIMARY HEAD INJURY Scalp injuries Skull fractures Extra-axial hemorrhages Intra-axial injuries Epidural hematoma Subdural hematoma Subarachnoid & intraventricular hemorrhage Epidural Hematoma (EDH) Epidural Hematoma (EDH) • Laceration or tearing of meningeal arteries • 90% arterial • 10% venous • YOUNG ADULTS, rare in elderly • M:F 4:1 Blood collection in space between inner table of skull and outer layer of dura Epidural Hematoma (EDH) NECT • ĂĐƵƚĞ͗аhyperdense͕ЫŵŝdžĞĚĚĞŶƐŝƚLJ • biconvex or lenticular-shaped • smooth • compresses underlying brain • midline shift • does not cross sutures (dura is attached to the calvarium tightly along the sutures) SWIRL SIGN •Internal hypodense component • Active bleeding with unretracted cloth Venous Epidural Hematoma Anterior temporal venous EDH • Adjacent to venous sinus • Fracture through sinus • Slow accumulation of blood • Can cross falx and tentorium Sphenoparietalal sinus Venous Vertex EDH Vertex Venous EDH Superior sagittal sinus Delayed Epidural Hematoma Therapy and prognosis of EDH • overall mortality 5%, bilateral EDH 15-20% • 10-25% will show enlargement within 1-36 h (“lucid interval” before it becomes large enough to cause unconsciousness) • majority require surgical evacuation • the bleeding stops when intracranial pressure exceeds arterial pressure At Presentation 24 Hours Later Subdural Hematoma (SDH) Subdural Hematoma (SDH) • Tearingng of bridgingbridging corticalcortical veinsveins • most common in ELDERLY • no gender predilection Blood collection in subdural space Subdural Hematoma (SDH) Subdural Hematoma (SDH) • Supratentorial convexity • Posterior fossa, along the falx • Adjacent to the tentorium Acute SDH > 1 week Subacute SDH 1-3 weeks Chronic SDH > 3 weeks Acute Subdural Hematomaa (aSDHH) • sickle-shaped, crescentic • 60% hyperdense • 40% mixed • smooth defined borders • may cross sutures • compression of the ventricle • midline shift • may have SWIRL SIGN “Subdural window setting” Window 150-300 HU Center/level 50-100 HU Subdural Hematoma (SDH) Isodense or hypodense aSDH • Anemia (low Hemoglobin) • Hematoma without clot • Tears in pia/arachnoid membrane result in CSF leakage into SDH = dilution • Coagulopathy CAVEAT! Subacutee Subdural Hematomaa (sSDHH) NECT • mixed density (recurrent hemorrhage) • gray-white junction displaced medially (“thick cortex”) • „dots“ of CSF = displaced cortical vessels CECT • enhancement of the dura and membranes Chronic Subdural Hematomaa (cSDHH) Chronic Subdural Hematomaa (cSDHH) NECT Homogenous/ Separated Trabecular laminar (hematocrit level) (internal septae, • sickle-shaped, crescentic calcifications) • MULTISEPTATED • variable density (mostly CSF density) • calcifications CECT • enhancement of the dura and membranes Chronic Subdural Hematomaa (cSDHH) Subdural Hygroma • traumatic tears in the What can happen to cSDH? arachnoid membrane Resolve spontaneously • usually 4-30 days (mean 9 Continue to grow days) after trauma Re-hemorrhage • Serum protein exsudation NO membranes • children: hematohygroma CSF collection in subdural space Subdural Hygroma Therapy and prognosis SDH • mortality 35-90% • hematoma thickness, midline shift > 2 cm requires surgical evacuation Subarachnoid Hemorrhage (SAH) Blood within subarachnoid spaces Traumaticraumatic Subarachnoid Subarachnoid Hemorrhage (SAB) Hemorrhage (SAH) • Tearing of vessels in subarachnoid space NECT • young age, chronic alcohol abuse • high density in subarachnoid spaces • M:F 2:1 • blood in interpeduncular cistern! • adjacent to contusions • Midline SAH is associated with DAI! • convexity > basal • Cause vasospasm much less frequently • focal or diffuse FLAIR is the most sensitive MRI technique in detection of SAH Susceptibilitytyy-weighted MR imaging Pseudodoo-SAH • Seen in diffuse brain edema • smooth-looking veins • Due to pial vessel engorgement and/or contraction of the subarachnoid space • rough boundary inhomogeneous SAH Wu Z et al. Evaluation of tSAH using SWI. AJNR 2010 Hasan TF et al. Journal of Stroke and Cerebrovascular Diseases 2018 Pseudodoo-SAH Intraventricularar Hemorrhage (IVH) • Seen with bilateral SDH • Rotationally induced tearing of subependymal veins on the ventral surface of the corpus callosum and along the fornix and septum pellucidum • spread from parenchymal bleed • retrograde influx of SAH 1. PRIMARY HEAD INJURY Scalp injuries Skull fractures Extra-axial hemorrhages Intra-axial injuries Cerebral Contusion Cerebral Contusion • Bruises of the brain parenchyma • Stationary head struck by object • Moving head (traffic, falls) • Can increase in size (first 48 h) • M:F 3:1 • children : adults 2:1 Brain surface injury involving gray matter and contiguous white matter Cerebral Contusion Cerebral Contusion Location COUP (blow) • anterior inferior frontal lobe • direct injury to brain beneath impact site • anterior inferior temporal lobe • brain hitting the interior of the skull • parietal/occipital lobes • posterior fossa CONTRECOUP (against the blow) • injury opposite impact site • due to process called cavitation Hemorrhagic Contusions Cerebral Hematoma • Collection of confluent, homogeneous blood in the brain parenchyma • Deeper part of the brain • Less edema Tonsillar hemorrhagic contusions after being hit with a baseball bat in the back of the head Contusion Hematoma Brain tissue and blood Blood “Release Hematoma” Diffuse axonal injury (DAI) • Shearing injuries resulting from abnormal rotation or deceleration of adjacent tissues that differ in density or rigidity • any age, most common young adults • M:F 2:1 When the head moves, the brain also moves. The different layers of the brain move at different times because each layer has a different density. Diffuse axonal injury (DAI) Diffuse axonal injury (DAI) • axons STRETCHED (rarely disconnected) • gray-white matter junction • metabolic alterations • frontal and temporal • cellular swelling • cytotoxic edema • corpus callosum (splenium) • apoptosis • brainstem (dorsolateral midbrain) • deep GM, internal capsule, fornix, corona radiata • cerebellar peduncle Diffuse axonal injury (DAI) Diffuse axonal injury (DAI) Adams and Gennarelli staging NECT MRI Stage 1 GM/WM junction (mild TBI) 50-80 % NORMAL multiple, small hypodense foci small focal lesions Stage 2 lobar WM, small hyperdense foci oval, elliptic corpus callosum (moderate TBI) 10-20% focal mass lesion punctate -15 mm Stage 3 midbrain, pons (severe TBI) Hemorrhagic Shearing Injuries Diffusiononn-weighted MR imaging a) Cytotoxic edema b) VasogenicVasogenic edemedemaa c) Central hemorrhage with cytotoxic edema Hergan K et al. Diffusion-weighted MRI in diffuse axonal injury of the brain. Eur Radiol 2002 DWI T2 GRE Splenial shear Courtesy T Huisman C/o J. Ocampo, Argentina Susceptibilitytyy-weighted MR imaging (SWI) GRE SWI Intermediary injuries Diffuse vascular injury (DVI) • Rare compared to DAI •Highimpact MVAs • 12% of fatal injuries • Immediate unconsciousness • Subcortical, deep WM, BG • A type of shearing injuries • Frontal, temporal lobes – Shearing of the perforating (lenticulostriate) arteries supplying the basal ganglia • Generally bilateral, asymmetrical • May have fluid/blood levels • Poor prognosis Courtesy Mauricio Castillo Courtesy of Anne Osborn 28 years-old male patient with head trauma, GCS=5 Courtesy Anne Osborn Diffuse vascular injury (DVI) • DVI and DAI are not separate entities but have a close relationship and that there may be a spectrum or at least a continuum between DAI and DVI • Hemorrhages are distrubuted along the perimedullary veins which drain into septal veins Missile and Penetrating Injuries Missile and Penetrating Injuries • Pressure wave in front of missile crushes / stretches tissue, creates temporary cavitation ENTRY SITE • soft tissue injury • Traumatic pseudoaneurysm • bone fragments • Vascular transection • bullet Cranial trauma from high-velocity projectile HEMORRHAGIC TRACT through brain (gunshot, sharp objects) HEMORRHAGES (SDH, EDH, SAH) EXIT SITE Arrow GSW Crowbar Knife Pencil Pen Pneumatic drill bit Arrow Picket fence Courtesy M Castillo.
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