Traumatic Brain Injury (TBI) Brain Trauma

Brain Trauma

Majda M Thurnher

• 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

Traumatic Brain Injury (TBI)

Glasgow Coma Scale

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):

Moderate Disability (9-12):Loss of consciousness greater than 30 minutesPhysical or cognitive impairments which may resolve

Severe Disability (3-8):Coma: unconscious state.No meaningful response, no voluntary activities

Vegetative State (Less Than 3):Sleep wake cyclesArousal, but no interaction with environmentNo localized response to pain

Classification of TBI

• Mechanism: closed or penetrating

• Severity: mild, moderate, severe

• Pathology: primary or secondary

• Morphology: focal or diffuse

1. PRIMARY HEAD INJURYScalp injuriesSkull fracturesExtra-axial hemorrhagesIntra-axial injuries

2. SECONDARY HEAD INJURYIschemiaHypoxiaHypotensionCerebral edemaMeningitis / AbscessIncreased intracranial pressure

Classification of TBI Primary brain injury refers to the sudden and profound injury to the brain that is considered to be more or less complete at the time of impact.

Secondary brain injury refers to the changes that evolve over a period of time (from hours to days) after the primary brain injury.

It includes an entire cascade of cellular, chemical, tissue, or blood vessel changes in the brain that contribute to further destruction of brain tissue.

1. PRIMARY HEAD INJURY

Scalp injuries

Skull fractures

Extra-axial hemorrhages

Intra-axial injuries

Epidural hematoma Subdural hematoma

Extra-axial hemorrhages

Subarachnoid &intraventricular hemorrhage

Epidural Hematoma (EDH)

Blood collection in space between inner table of skull and outer layer of dura

• Laceration or tearing of meningeal arteries• 90% arterial • 10% venous

• YOUNG ADULTS, rare in elderly• M:F 4:1

Epidural Hematoma (EDH)

NECT• hyperdense• biconvex or lenticular-shaped• smooth• compresses underlying brain• midline shift• does not cross sutures

(dura is attached to the calvarium tightly along the sutures)

Epidural Hematoma (EDH)

• Internal hypodense component

• Active bleeding with unretractedcloth

SWIRL SIGN

• Adjacent to venous sinus• Fracture through sinus• Slow accumulation of blood • Can cross falx and tentorium

Venous Epidural Hematoma Anterior temporal venous EDH

Sphenoparietalal sinus

Vertex Venous EDH

Superior sagittal sinus

Venous Vertex EDH

Delayed Epidural Hematoma

At Presentation 24 Hours Later

• 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

Therapy and prognosis of EDH

Blood collection in subdural space

Subdural Hematoma (SDH) • Tearing of bridging cortical veins• most common in ELDERLY

• no gender predilection

ng of bridging cortical veinsSubdural Hematoma (SDH)

• Supratentorial convexity• Posterior fossa, along the falx • Adjacent to the tentorium

Subdural Hematoma (SDH)

Acute SDH > 1 week

Subacute SDH 1-3 weeks

Chronic SDH > 3 weeks

Subdural Hematoma (SDH)

• sickle-shaped, crescentic • 60% hyperdense• 40% mixed • smooth defined borders• may cross sutures• compression of the ventricle• midline shift• may have SWIRL SIGN

Acute Subdural Hematoma (a (aSDHH)

“Subdural window setting”

Window 150-300 HU

Center/level 50-100 HU

Isodense or hypodense aSDH

• Anemia (low Hemoglobin)• Hematoma without clot• Tears in pia/arachnoid membrane result in CSF

leakage into SDH = dilution • Coagulopathy

Subdural Hematoma (SDH)

CAVEAT!

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

Subacutee Subdural Hematoma (a (sSDHH)

NECT• sickle-shaped, crescentic • MULTISEPTATED• variable density (mostly CSF density)• calcifications

CECT• enhancement of the dura and membranes

Chronic Subdural Hematoma (a (cSDHH)

Homogenous/ laminar

Chronic Subdural Hematoma (a (cSDHH)

Separated (hematocrit level)

Trabecular (internal septae, calcifications)

What can happen to cSDH?

Resolve spontaneously

Continue to grow

Re-hemorrhageSerum protein exsudation

Chronic Subdural Hematoma (a (cSDHH)

CSF collection in subdural space

Subdural Hygroma

• traumatic tears in the arachnoid membrane

• usually 4-30 days (mean 9 days) after trauma

• NO membranes• children: hematohygroma

Subdural Hygroma

• mortality 35-90%• hematoma thickness, midline shift > 2 cm

requires surgical evacuation

Therapy and prognosis SDH

Blood within subarachnoid spaces

Subarachnoid Hemorrhage (SAH)

• Tearing of vessels in subarachnoid space• young age, chronic alcohol abuse• M:F 2:1

• Midline SAH is associated with DAI!

• Cause vasospasm much less frequently

Traumatic Subarachnoid raumatic SubarachnoidHemorrhage (SAH)

NECT• high density in subarachnoid spaces• blood in interpeduncular cistern!• adjacent to contusions• convexity > basal

• focal or diffuse

Subarachnoid Hemorrhage (SAB)

FLAIR is the most sensitive

MRI technique in detection of SAH

Wu Z et al. Evaluation of tSAH using SWI. AJNR 2010

• smooth-looking veins• rough boundaryinhomogeneous SAH

Susceptibilityty-y-weighted MR imaging Pseudodo-o-SAH • Seen in diffuse brain edema• Due to pial vessel engorgement and/or

contraction of the subarachnoid space

Hasan TF et al. Journal of Stroke and Cerebrovascular Diseases 2018

Pseudodo-o-SAH • 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

Intraventricularar Hemorrhage (IVH)

1. PRIMARY HEAD INJURY

Scalp injuries

Skull fractures

Extra-axial hemorrhages

Intra-axial injuries

Brain surface injury involving gray matter and contiguous white matter

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

Cerebral Contusion

Location• anterior inferior frontal lobe• anterior inferior temporal lobe• parietal/occipital lobes• posterior fossa

Cerebral Contusion

COUP (blow)

• direct injury to brain beneath impact site• brain hitting the interior of the skull

CONTRECOUP (against the blow)

• injury opposite impact site• due to process called cavitation

Cerebral Contusion

Hemorrhagic Contusions

Tonsillar hemorrhagic contusions after being hit with a baseball bat in the back of the

head

Cerebral Hematoma

• Collection of confluent, homogeneous blood in the brain parenchyma

• Deeper part of the brain

• Less edema

Brain tissue and blood Blood

Contusion Hematoma

“Release Hematoma”

• 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)

• axons STRETCHED (rarely disconnected)

• metabolic alterations• cellular swelling• cytotoxic edema • apoptosis

Diffuse axonal injury (DAI)

• gray-white matter junction• frontal and temporal• corpus callosum (splenium)• brainstem (dorsolateral midbrain)

• deep GM, internal capsule, fornix, corona radiata• cerebellar peduncle

Diffuse axonal injury (DAI)

Adams and Gennarelli staging

Stage 1 GM/WM junction (mild TBI)

Stage 2 lobar WM, corpus callosum (moderate TBI)

Stage 3 midbrain, pons (severe TBI)

Diffuse axonal injury (DAI)

NECT50-80 % NORMALsmall hypodense foci

small hyperdense foci

10-20% focal mass lesion

MRImultiple,

small focal lesions

oval, elliptic

punctate -15 mm

Diffuse axonal injury (DAI)

Hemorrhagic Shearing Injuries

Hergan K et al. Diffusion-weighted MRI in diffuse axonal injury of the brain. Eur Radiol 2002

Diffusionon-n-weighted MR imaging

a) Cytotoxic edemaa)b)

Cytotoxic edemaVasogenic edemab)

c)Vasogenic edemaCentral hemorrhage with cytotoxic edema

GRE

T2

DWI

Courtesy T Huisman

Splenial shear

C/o J. Ocampo, Argentina

Susceptibilityty-y-weighted MR imaging (SWI)

GRE SWI

Courtesy Mauricio Castillo

• A type of shearing injuries– Shearing of the perforating (lenticulostriate) arteries

supplying the basal ganglia

• Generally bilateral, asymmetrical• May have fluid/blood levels• Poor prognosis

Intermediary injuries

• Rare compared to DAI• High impact MVAs• 12% of fatal injuries• Immediate unconsciousness• Subcortical, deep WM, BG• Frontal, temporal lobes

Courtesy of Anne Osborn

Diffuse vascular injury (DVI)

Courtesy Anne Osborn28 years-old male patient with head trauma, GCS=5

• DVI and DAI are not separate entities but have a closerelationship and that there may be a spectrum or at least a continuum between DAI and DVI

Diffuse vascular injury (DVI)

• Hemorrhages are distrubutedalong the perimedullary veinswhich drain into septal veins

Missile and Penetrating Injuries

Cranial trauma from high-velocity projectile (gunshot, sharp objects)

• Pressure wave in front of missile crushes / stretches tissue, creates temporary cavitation• Traumatic pseudoaneurysm• Vascular transection

ENTRY SITE • soft tissue injury• bone fragments• bullet

HEMORRHAGIC TRACT through brain

HEMORRHAGES (SDH, EDH, SAH)

EXIT SITE

Missile and Penetrating Injuries

Arrow

GSW

Pencil Pen

KnifeCrowbar

Arrow Picket fence

Pneumatic drill bit

Courtesy M Castillo