imaging of the traumatic brain injury by rathachai kaewlai, md

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Imaging of Traumatic Brain Injury

Rathachai Kaewlai, MD Ramathibodi Hospital, Mahidol University, Bangkok Emergency Radiology Minicourse 2013 Slides available at RiTradiology.com or Slideshare.net/rathachai


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Outline •  Background of traumatic

brain injury (TBI) •  Imaging modalities

–  CT –  X-ray –  MRI

•  Clinical prediction rules

•  Primary lesions –  Intraaxial hemorrhages –  Extraaxial hemorrhages

•  Secondary lesions


Traumatic Brain Injury (TBI)

•  Leading cause of death and disability •  Major risk factors: extreme age, male,

low socioeconomic status •  Mortality related to Glasgow Coma Scale

(GCS) score

Head injury classified by GCS 13-15 = mild HI 8-12 = moderate HI 7 or less = severe HI



•  Closed or open? It depends on dura integrity

Closed Open More common Less common

Dura intact Dura disrupted

Violent accelerations of brain tissue (coup-contrecoup)

Fracture or FB penetrating dura



•  Primary or secondary brain lesions? It’s “how” closely lesions are linked to traumatic event

Primary Secondary Caused by trauma itself Processes arising from 1) brain’s

responses to trauma 2) compression of brain, CN, BV, skull and dura

Less devastating More devastating Skull fractures, extraaxial hemorrhages, intraaxial lesions (DAI, contusion, IVH)

Herniations, diffuse edema, infarction and infarction

DAI = Diffuse axonal injury, IVH = intraventricular hemorrhage, CN = cranial nerves, BV = blood vessels


Goals of Imaging in TBI Goals Answered by... Rapid diagnosis of life-threatening injuries

Explanation of neurological abnormality

Prognosis information

CT

CT (if not MRI)

Clinical findings, CT, MRI, advanced MR techniques


CT in TBI: Why?

•  Widely available •  Fast •  Sensitive for detection and evaluation of

injuries requiring acute neurosurgical intervention

  Deciding whether surgical or medical Rx

Image from salvationist.ca


CT in TBI: When?

•  Moderate & severe acute closed HI •  Minor acute closed head injury with…

– Risk factors* or – Neurological deficit present

•  Children <2 years old •  Penetrating injury •  Skull fracture •  R/O carotid or vertebral artery injury

HI = head injury


CT in TBI: When?

•  Patients with mild HI with one of 7 clinical findings need CT: –  Short-term memory deficit –  Drug/alcohol intoxication –  Physical evidence of trauma

above clavicles –  Age > 60 –  Seizure –  Headache –  Vomiting

NEJM 2000

New Orleans Criteria Using this scheme, CT

positivity rate was about 7-10%

Sensitivity = 100%


CT in TBI

•  Sensitivity for predicting need for neurosurgery –  High risk 100% –  Medium risk 98.4%

•  Reduced the need for CT in mild HI to 54%

•  Positivity rate = 8% (1% of cases require neurosurgical intervention)

Stiell IG, et al. Lancet 2001;357:1391-96. | Diagram from ohri.ca


CT in TBI: How? •  Non-contrast, axial scan with spiral technique •  At our hospital, we use 3 mm slice thickness and

alway do bone algorithm, coronal/sagittal reformations

•  If you see maxillary hemosinus do facial CT •  If you see skull base fracture consider CTA

and skull base reformation (thin slices with small FOV)

•  If suspect C-spine fracture do C-spine CT


CT in TBI: Checklist

•  Look at all three windows

Brain Subdural Bone


CT in TBI: Checklist •  Look for primary lesions •  Don’t forget secondary lesions (they may

be more catastrophic) •  If the study looks near-normal

–  Find coup injury look for contrecoup (can be subtle)

–  Check potential areas for contusions and DAI (esp if low GCS)

•  Recheck interpeduncular fossa for small SAH


Skull X-ray: Outdated Yet? •  No! •  Penetrating injury •  Radiopaque foreign bodies e.g. GSW •  Part of skeletal survey in cases suspecting

child abuse •  Caveats: Skull fractures...

– About 1/3 of cases with severe TBI do not have skull fracture!

– Negative skull x-ray does not mean no CT


Skull X-ray: How? •  Skull trauma series in adults should

include at least 3 views given complex skull bones – Frontal – Lateral – Towne’s

•  Learn to find fractures and distinguish them from mimics


MRI in TBI: Pros

•  More sensitive for 10 and 20 injuries than CT •  Better differentiation of hemorrhagic and

non-hemorrhagic lesions in acute phase

Same-day MRI

Diffuse axonal injury


MRI in TBI: Cons

•  Intrinsic limits: –  Absolute C/I: cardiac pacemaker, ferromagnetic foreign

bodies –  Lower sensitivity for bone fractures and hyperacute blood

•  Difficult managing trauma patients in MRI suite: metallic life support, monitoring device, time

T1 T2 FLAIR CT Images from Scarabino, et al. Emergency Neuroradiology, 2006


SKULL FRACTURE


Quick Anatomy

•  3 layers –  Outer table –  Diploe –  Inner table

•  Parts without diploe prone to fracture –  Squamous temporal bone / Parietal bone –  Foramen magnum, skull bases, cribiform plates,

orbital roofs


Quick Anatomy

(c) 2003 Encyclopedia Brittanica


Quick Anatomy


Types of Skull Fracture •  Linear fracture

–  a/w EDH, SDH •  Depressed fracture

–  a/w focal parenchymal lesions

•  Skull base fracture •  Open head injuries

–  Knife, firearm –  Laceration of dura www.uchospitals.edu


Significance of Skull Fracture •  Indicator of brain injuries?...Not quite

– Present in the majority of cases with severe HI

– Absent in 1/4 of fatal injuries at autopsy – Absent in 1/3 of severe brain injury cases

•  Injuries to underlying brain structures •  Association

– 15% concomitant C-spine injury – 10-15% concomitant facial injury


Skull Fracture: Imaging

•  Best = Helical CT scan with multiplanar reformation (MPR)

In-plane fracture easier to see on reformats


Skull Fracture: Imaging •  Bone window with edge enhancement algorithm

Soft tissue algorithm Bone algorithm


Skull Fracture: Difficulty on XR

Window level adjusted Routine window


Skull Fracture vs. Suture FRACTURE SUTURE Smooth or jagged edge Serrated edge Straight line Curvilinear line Angular turn Curvilinear turn Greater in width Lesser in width (X-ray) darker (X-ray) lighter Any locations Specific anatomic location


Skull Fracture: Difficulty on CT

Use subgaleal hematoma as a clue


Skull Fracture: Diastatic

•  Fracture along suture lines “traumatic sutural separation” •  Usually affected newborns and infants (unfused sutures) •  Commonly unilateral •  Most common location = lambdoid and sagittal sutures •  >2 mm separation that is asymmetric


Skull Fracture: Depressed •  In adults, criteria to elevate:

–  >8-10 mm depression or >1 thickness of skull

–  Deficit related to underlying brain –  CSF leak

•  In children, two types: –  Simple depressed: usually

remodelling occurs with growth, surgery if dura penetrated or persistent cosmetic defect

–  Ping-pong ball fractures: Rx if underlying brain injury or dura penetrated


Skull Fracture: Skull Base •  Most are extensions of

fracture of cranial vault •  Clinical clues:

–  CSF otorrhea or rhinorrhea –  Hemotympanum or laceration of

EAC –  Postauricular ecchymoses –  Periorbital ecchymoses in

absence of direct orbital trauma esp if bilateral

–  Cranial nerve injury (I, VI, VII, VIII)

Longitudinal


Skull Fracture: Skull Base •  Thin slices, bone

algorithms and coronal images needed for Dx

•  Indirect CT signs: –  Pneumocephalus –  Air-fluid level or

opacification of mastoid or sinuses

Longitudinal Oblique


Skull Fracture: Missile Injuries Depressed Penetrating Perforating Missile not penetrate skull but produces depressed fx or brain contusion

Missile enters cranial cavity but does not leave it

Missile enters and exits cranial cavity

Focal brain damage

Injury depends on damage to vital structures

Most severe injury due to shockwaves generated by missiles

Foreign body, meningitis, abscesses

Foreign body, meningitis, abscesses


Skull Fracture: Pneumocephalus •  Gas within cranial cavity •  In acute trauma setting, this is

commonly due to fractures of PNS and temporal bones (open skull fracture is another cause)

•  Most do not cause immediate danger but rapid expansion can lead to brain compression (tension pneumocephalus)

–  Mount Fuji sign

•  Usually decreases by 10-15 days and almost never present by 3 weeks


DIFFUSE AXONAL INJURY


Diffuse Axonal Injury (DAI)

•  Traumatic acceleration/deceleration or violent rotation

•  LOC immediately at the time of trauma coma •  Most severe of all primary brain lesions

Images from http://www.pathguy.com/bryanlee/dai.htm


Diffuse Axonal Injury (DAI)

•  Frequent cause of persistent vegetative state / morbidity in trauma patients

•  Clinical symptoms worse than CT findings

•  Can be isolated with no or little association with SAH, SDH, fracture


Diffuse Axonal Injury

•  Non-hemorrhagic 80% of cases •  Common locations:

–  Grey-white matter interface (m/c) –  Corpus callosum –  Dorsolateral midbrain

•  Number and location of lesions predict prognosis (worse if multiple & supratentorial)

•  MRI most sensitive imaging but still underestimates real extent

Susceptibility-weighted MRI

CT


Diffuse Axonal Injury

•  When initial head CT is normal but the patient is in vegetative state – Do MRI with susceptibility sequence OR – Follow up CT in 24 hours (1/6 of DAI will

evolve)

Small interpeduncular SAH and petechial hemorrhage in dorsolateral midbrain on CT and susceptibility-weighted MRI


CEREBRAL CONTUSION


Cerebral Contusion

•  Cerebral gyri impact inner table skull •  Characterizes coup and contrecoup

injuries •  Petechial hemorrhage of gyri small

hemorrhage large hematoma

Images from Wikipedia.org


Cerebral Contusion

•  Anterior base frontal, temporal lobes (esp tip), cortex surrounding Sylvian fissure

•  Multiple, bilateral


Cerebral Contusion

•  Can be normal early; can be non-hemorrhagic •  Imaging worsened with time, most evident after 24 h

Day 0 Day 1


Cerebral Contusion: MRI

FLAIR T2W

MRI is the study of choice in patients with •  Acute TBI when neurological findins are unexplained by CT •  Subacute or chronic phases when there are TBI-related symptoms


OTHER INTRAAXIAL LESIONS

Traumatic intraparenchymal hematoma Intraventricular hemorrhage Traumatic lesions of deep grey structures and brainstem


Intraparenchymal Hematoma •  Parenchymal vessel

rupture from blunt or penetrating forces

•  May not lose consciousness (unlike DAI, contusion)

•  Hematoma at primary trauma site (usually frontal and temporal)


Intraparenchymal Hematoma

•  Well-circumscribed hyperdense lesion w/wo perilesional edema

•  Up to 60% a/w SDH, EDH •  Not always easy to

distinguish IPH from DAI or contusion

Traumatic intraparenchymal hemorrhage with IVH


Intraventricular Hemorrhage

•  Uncommon •  Consequence of severe trauma. a/w DAI and

trauma of deep grey and brainstem •  Poor prognosis


Trauma of Deep Grey & Brainstem •  Stretch and torsion causing ruptured perforators,

or direct impact on dorsolateral brainstem against tentorial incisura

•  Severe trauma, poor prognosis •  CT:

–  Small hemorrhages in brainstem surrounding aqueduct, basal grey nuclei

–  Can be normal


EPIDURAL HEMATOMA


Epidural Hematoma (EDH)

•  Hematoma between inner table of the skull and dura

•  Source of bleeding –  Most common = middle

meningeal artery (90%) (squamous temporal bone)

–  Venous EDH from dural venous sinus

www.practicalhospital.com


Epidural Hematoma (EDH) •  Most urgent of all cases of cranial trauma

–  Requiring prompt Rx to relieve compression of brainstem, tentorial herniation, acute hydrocephalus

–  EDH in posterior fossa very worrisome

•  1-4% of head injury cases, 10% of fatal cases •  Young men (20s – 40s). Rare in patients >60 y •  Almost always with skull fracture •  Lucid interval in 40% of cases


Epidural Hematoma (EDH)

•  Delayed development in 10-25% of cases (within 36 hrs) – Arterial EDH: blood can flow into epidural

space only after resolution of arterial spasm – Venous EDH bleeds slowly


Epidural Hematoma: CT Appearance •  Biconvex or lens shape

hyperdense lesion (rare to be isodense)

•  May cross midline and dural attachment

•  Do not cross suture (except diastatic fracture, large EDH)


Epidural Hematoma: Potential Indications for Surgery •  Size > 2 cm •  Active bleeding •  Impending herniation •  Corresponding

neurologic deficit


Epidural Hematoma: Swirl Sign

•  First described by Zimmerman in 1982

•  Small rounded lesion isodense to the brain, representing active extravasation of unclotted blood

•  Clotted component is hyperdense (50-70 HU)


Venous EDH •  Tear of venous sinus

(high flow, low pressure system)

•  More benign course, subacute presentation, usually not require surgery

•  Posterior fossa venous sinus > sagittal sinus


SUBDURAL HEMATOMA


Subdural Hematoma (SDH)

•  Blood collects between dura and arachnoid

•  Torn cortical bridging veins •  10-20% of all cranial

trauma cases •  Demographics:

–  Elderly (60-80y) with brain atrophy,

–  Large intracranial subarachnoid spaces

–  “Shaken baby syndrome”

www.nucleusinc.com


Subdural Hematoma (SDH)

•  Usually co-exist with other brain injuries –  Esp. contusion-typed

injuries > skull fractures •  Acute: within 3 days

from trauma •  Subacute: within 3 mo •  Chronic: after 3 months

Layer of acute blood on pre-existing CSF-like subdural collection in the right cerebral convexity


Subdural Hematoma: CT Appearance •  Crescentic hyperdense

collection •  Can cross suture •  Can extend to

interhemispheric fissure, along tentorium cerebelli

Note coup (Rt.) and contrecoup (Lt.) pattern. This SDH is a contrecoup injury.


Subdural Hematoma: Value of Coronal Reformats


Bilateral Subdural Hematomas

Don’t feel “enough” with trauma findings. There’re almost always more to be discovered.


“Isodense” Subdural Hematoma

•  Usually takes 2-6 weeks for acute SDH to become isodense

•  At Hb 8-10 g/dL, blood will be isodense to grey matter

•  Anemic patients can present with acute isodense SDH


Acute On Chronic SDH

•  New hemorrhage superimposed on chronic SDH

•  Recurrent trauma •  Can be spontaneous •  Blood-fluid level , blood

clot organization, membranes


Comparison of EDH and SDH

EDH SDH Incidence 1-4% of trauma cases;

10% of fatal trauma cases 10-20% of all trauma cases; 30% of fatal trauma cases

Etiology a/w fractures in 90% of cases Laceration of MMA/venous sinus

Tearing of cortical veins

Site Between skull and dura 95% supratentorial

Between dura and arachnoid 95% supratentorial

Crosses dura but not sutures Crosses suture but not dura CT findings Biconvex (lens) shape

Shift grey-white matter interface Crescentic shape

Diagram from Kumar et al. Basic Pathology 7E


Subdural Hygroma

•  Extraaxial collection of CSF caused by extravasation of CSF from SA space through a traumatic tear in arachnoid mater

•  Acute: Children >> adults •  Subacute and chronic:

Following surgery for head injuries in operative bed or opposite site

1 week after injury

Day of injury


TRAUMATIC SUBARACHNOID HEMORRHAGE (TSAH)


Subarachnoid Hemorrhage (SAH) •  Blood collects beneath

arachnoid •  Tear of veins in SA space •  Usually associated with

other brain injuries (common with contusions)

•  ‘Nearly all cases of traumatic SAH have other lesions to suggest traumatic cause’ –  Isolated SAH in trauma

patients – possible ruptured aneurysm causing trauma

SAH with SDH


Subarachnoid Hemorrhage •  Site

–  Next to brain contusion, under SDH/fracture/scalp lac

–  Can be distant because blood diffuses in SA space

•  IVH may co-exist due to retrograde flow through foramen of Luschka and Magendie

SAH with contusion


Subarachnoid Hemorrhage

•  Subtle SAH – interpeduncular fossa


TRAUMATIC VASCULAR LESIONS

ICA dissection Carotid-cavernous fistula (CCF)


Traumatic Vascular Lesions

•  Rare •  Can be overlooked initially •  ICA injury (dissection, aneurysm, occlusion)

–  Base of skull fracture

•  Traumatic carotid-cavernous fistula (TCCF)


Traumatic ICA Injury •  Common cause of

ischemic stroke in the young

•  Extracranial ICA much more common (esp just proximal to petrous bone)

•  Dissection occlusion or thromboembolism

At initial trauma, there were diffuse subarachnoid hemorrhage, pneumocephalus, facial fractures and C-spine injury. Days after the injury (image C) , the patient developed left ICA territory

infarction. Angiiography (D) confirmed occlusion of the cervical ICA. Images from Yang S, et al. J Clin Neurosci 2006;13:123


Traumatic CCF

•  Most common traumatic AV fistula = CCF –  Clues on CT: proptosis, bulging cavernous sinus, enlarged-

arterialized ophthalmic vein

A vividly enhancing structure in the right cavernous sinus with a dilated superior ophthalmic vein. Note right proptosis


SECONDARY LESIONS

Herniation Cerebral edema Ischemia and infarction Secondary hemorrhage Hydrocephalus Brain death


Herniation

•  Supra- and infratentorial cranial compartments by dura and bones

•  Expanding lesion mechanical shift of cerebral parenchyma, CSF and attached BV from one compartment to another Wikipedia.org


Herniation Herniation Clinical Findings Imaging Findings Where to

Look? Complications

Descending transtentorial

•  Ipsilated dilated pupil •  Contralateral hemiparesis •  Ipsilateral hemiparesis (if Kernohan notch is present)

•  Uncus extending into suprasellar cistern •  Widening of ipsilateral ambient and prepontine cisterns •  Widening of contralateral temporal horn

Midbrain Occipital infarct from PCA compression

Ascending transtentorial

•  Nausea •  Vomitting •  Obtundation

•  Spinning top appearance of midbrain •  Narrow bilateral ambient cisterns •  Filling of quadrigeminal plate cistern

Midbrain and associated cisterns

Hydrocephalus Rapid onset obtundation and possible death

Alar (sphenoid)

•  None •  Displacement of MCA on axial views •  Distorted insular cortex on sagittal views

MCA None

Subfalcine •  Headache •  Contralateral leg weakness

•  Asymmetric anterior falx •  Obliterated ipsilateral frontal horn and atrium of lateral ventricle •  Septum pellucidum shift

Septum pellucidum at level of foramen of Monro

Ipsilateral ACA infarction

Tonsillar •  Bilateral arm dysesthesia •  Obtundation

•  Tonsils at level of dens on axial •  Tonsils on sagittal 5mm below foramen magnum (adult); 7mm below (children)

Foramen magnum on axials and sagittals

Obtundation Death


Herniation: Tonsillar

•  Downward displacement of tonsils through foramen magnum

•  Seen with –  Up to ½ of all descending transtentorial herniation –  Up to 2/3 of ascending transtentorial herniation


Herniation: Subfalcine and Midline Shift •  Shift of cingulate gyrus across midline below falx •  Thinner ipsilateral ventricle, dilated opposite

ventricle (CSF obstruction at foramen of Monro)


Herniation: Subfalcine and Midline Shift •  Measured at level of foramen of Monro •  Distal ACA may be compressed against falx


Herniation: Descending Transtentorial •  Medial and caudal shift

of uncus and parahippocampal gyrus of temporal lobe beyond tentorium cerebelli

•  Asymmetric prepontine cisterns and CP angle (wider on side of lesion)

•  AchA, PCoA, PCA may be compressed against tentorium


Herniation: Descending Transtentorial

Before surgery After surgery


Herniation: Ascending Transtentorial •  Cranial shift of vermis and

parts of superomedial cerebellar hemisphere through tentorium incisura

•  Compressed superior cerebellar, vermian cisterns and forth ventricle


Posttraumatic Cerebral Edema

•  Increased water content of brain and/or increased intravascular blood volume

•  Severe condition. Can be fatal •  Can be unilateral or bilateral •  Vasogenic and cytotoxic edema coexist

(vasogenic immediately, then cytotoxic) •  Evolves over 24-48 hours •  Generally resolved in 2 weeks


Posttraumatic Cerebral Edema

•  Generalized obliteration of cortical sulci and SA spaces of suprasellar, perimesencephalic and compressed/thin ventricles

•  Diffuse hypodensity, loss of grey-white matter interface

•  Hyperdense cerebellum •  Often w/ transtentorial

herniation


Posttraumatic Ischemia/Infarct

•  m/c cause = herniation •  m/c location = occipital

(PCA infarct from descending transten)

•  2nd m/c location = frontal (ACA infarct from subfalcine h)

•  Rare = basal ganglia (perforator/choroidal infarct against base skull)

3 months later

At time of trauma


Posttraumatic Secondary Hemorrhages •  Small hemorrhagic foci in

tegmen = Duret hemorrhage –  Classic in midline of

pontomesencephalic junction –  May be multiple or extending

into cerebellar peduncles •  Necrosis/hemorrhage of

contralateral cerebral peduncle = Kernohan’s notch “false localizing sign”

Hemorrhage in the midline near pontomesencephalic junction. Also note

intraventricular hemorrhage in the 4th ventricle


Hydrocephalus •  Acute hydrocephalus can

occur 2/2 brain herniation or IVH

•  Delayed hydrocephalus usually 2/2 adherence of meninges over cerebral convexity, basal cisterns or aqueduct resulting in obstruction at level of ventricles and arachnoid granulations

Look for “early sign” of hydrocephalus at temporal horns of lateral ventricles. When acute with high ICP, there may be hypodensity around the frontal horns of lateral ventricles


Brain Death •  Severe increased ICP

decreases cerebral blood flow, then irreversible loss of brain function

•  Clinical criteria: coma + absent brainstem reflexes + apnea test

•  No flow in intracranial arteries/venous sinuses

•  Diffuse cerebral edema, hyperdense cerebellum

Pseudo-SAH with non-visualization of contrast enhancement of intracranial vessels. Only external carotid arterial branches are enhanced


Conclusions

•  CT = primary modality for head trauma, enough for most parts – Skull x-rays still used in penetrating trauma,

suspected child abuse – MR to help predicting prognosis by detection

of subtle injuries i.e., contusion and DAI •  Primary vs secondary lesion. Often,

secondary lesion more important


Conclusions

•  While checking the scan, make sure to think if the patient needs CTA or other CTs (C-spine, facial bones, etc)

•  Coup-contrecoup mechanism helps confirm acute trauma nature and search for subtle lesions

imaging of the traumatic brain injury by rathachai kaewlai, md

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