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Imaging of Traumatic Brain Injury www.RiTradiology.com 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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Disclaimer www.RiTradiology.com All opinions expressed here are those of the authors and not of their employers. Information provided here is for medical education only. It is not intended as and does not substitute for medical advice. If you are a patient, please see your doctor for evaluation of your individual case. Under no circumstances will the authors be liable to you for any direct or indirect damages arising in connecting with the use of this website. The presentation may contain links to third party web sites. This does not constitute endorsement, guarantee, warrantee or recommendation by the authors. We do not verify, endorse, or take responsibility for the accuracy, currency, completeness or quality of the content contained in these sites. There is no real life patient data on this presentation. We do not write about patients. All case descriptions are fictional, similar to descriptions you can find in a multiple choice questions textbook for examination preparation.
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Outline www.RiTradiology.com Background of traumatic brain injury (TBI) Imaging modalities CT X-ray MRI Clinical prediction rules Primary lesions Intraaxial hemorrhages Extraaxial hemorrhages Secondary lesions
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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 www.RiTradiology.com 13-15 8-12 7 or less = mild HI = moderate HI = severe HI
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Traumatic Brain Injury (TBI) www.RiTradiology.com Closed or open? It depends on dura integrity
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Traumatic Brain Injury (TBI) www.RiTradiology.com Primary or secondary brain lesions? It’s “how” closely lesions are linked to traumatic event DAI = Diffuse axonal injury, IVH = intraventricular hemorrhage, CN = cranial nerves, BV = blood vessels
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Goals of Imaging in TBI www.RiTradiology.com
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www.RiTradiology.com 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
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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 www.RiTradiology.com HI = head injury
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www.RiTradiology.com 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%
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www.RiTradiology.com 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
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CT in TBI: How? www.RiTradiology.com 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
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CT in TBI: Checklist Look at all three windows Brain www.RiTradiology.com Subdural Bone
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CT in TBI: Checklist www.RiTradiology.com 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
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Skull X-ray: Outdated Yet? www.RiTradiology.com 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
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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 www.RiTradiology.com
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www.RiTradiology.com 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
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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 CT T1 T2 FLAIR www.RiTradiologyI.cmomages from Scarabino, et al. Emergency Neuroradiology, 2006
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SKULL FRACTURE www.RiTradiology.com
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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 www.RiTradiology.com
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Quick Anatomy www.RiTradiology.com (c) 2003 Encyclopedia Brittanica
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Quick Anatomy www.RiTradiology.com
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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 www.RiTradiology.com
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Significance of Skull Fracture www.RiTradiology.com 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
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www.RiTradiology.com Skull Fracture: Imaging Best = Helical CT scan with multiplanar reformation (MPR) In-plane fracture easier to see on reformats
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Skull Fracture: Imaging Bone window with edge enhancement algorithm Soft tissue algorithm Bone algorithm www.RiTradiology.com
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Skull Fracture: Difficulty on XR Window level adjusted www.RiTradiology.com Routine window
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Skull Fracture vs. Suture www.RiTradiology.com
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Skull Fracture: Difficulty on CT Use subgaleal hematoma as a clue www.RiTradiology.com
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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 www.RiTradiology.com
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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 www.RiTradiology.com
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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 www.RiTradiology.com
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Skull Fracture: Skull Base Thin slices, bone algorithms and coronal images needed for Dx Indirect CT signs: – Pneumocephalus Longitu–diAnairl -fluid level or opacification of mastoid or sinuses Oblique www.RiTradiology.com
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Skull Fracture: Missile Injuries www.RiTradiology.com
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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 www.RiTradiology.com
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DIFFUSE AXONAL INJURY www.RiTradiology.com
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www.RiTradiology.c om 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
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www.RiTradiology.com 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
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www.RiTradiology.com 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
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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) www.RiTradiology.com Small interpeduncular SAH and petechial hemorrhage in dorsolateral midbrain on CT and susceptibility-weighted MRI
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www.RiTradiology.com CEREBRAL CONTUSION
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www.RiTradiology.com 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
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www.RiTradiology.com Cerebral Contusion Anterior base frontal, temporal lobes (esp tip), cortex surrounding Sylvian fissure Multiple, bilateral
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www.RiTradiology.com Cerebral Contusion Can be normal early; can be non-hemorrhagic Imaging worsened with time, most evident after 24 h Day 0 Day 1
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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 www.RiTradiology.com
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OTHER INTRAAXIAL LESIONS www.RiTradiology.com Traumatic intraparenchymal hematoma Intraventricular hemorrhage Traumatic lesions of deep grey structures and brainstem
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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) www.RiTradiology.com
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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 www.RiTradiology.com
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Intraventricular Hemorrhage Uncommon Consequence of severe trauma. a/w DAI and trauma of deep grey and brainstem Poor prognosis www.RiTradiology.com
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Trauma of Deep Grey & Brainstem www.RiTradiology.com 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
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EPIDURAL HEMATOMA www.RiTradiology.com
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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 www.RiTradiology.com
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Epidural Hematoma (EDH) www.RiTradiology.com 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
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Epidural Hematoma (EDH) www.RiTradiology.com 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
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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) www.RiTradiology.com
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Epidural Hematoma: Potential Indications for Surgery Size > 2 cm Active bleeding Impending herniation Corresponding neurologic deficit www.RiTradiology.com
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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) www.RiTradiology.com
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Venous EDH www.RiTradiology.com Tear of venous sinus (high flow, low pressure system) More benign course, subacute presentation, usually not require surgery Posterior fossa venous sinus > sagittal sinus
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SUBDURAL HEMATOMA www.RiTradiology.com
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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 www.RiTradiology.com
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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 www.RiTradiology.com
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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. www.RiTradiology.com
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Subdural Hematoma: Value of Coronal Reformats www.RiTradiology.com
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Bilateral Subdural Hematomas www.RiTradiology.com Don’t feel “enough” with trauma findings. There’re almost always more to be discovered.
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“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 www.RiTradiology.com
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Acute On Chronic SDH New hemorrhage superimposed on chronic SDH Recurrent trauma Can be spontaneous Blood-fluid level , blood clot organization, membranes www.RiTradiology.com
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Comparison of EDH and SDH www.RiTradiology.com Diagram from Kumar et al. Basic Pathology 7E
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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 www.RiTradiology.com 1 week after injury Day of injury
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TRAUMATIC SUBARACHNOID HEMORRHAGE (TSAH) www.RiTradiology.com
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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 www.RiTradiology.com
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www.RiTradiology.com 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
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Subarachnoid Hemorrhage Subtle SAH – interpeduncular fossa www.RiTradiology.com
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TRAUMATIC VASCULAR LESIONS www.RiTradiology.com ICA dissection Carotid-cavernous fistula (CCF)
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Traumatic Vascular Lesions www.RiTradiology.com Rare Can be overlooked initially ICA injury (dissection, aneurysm, occlusion) – Base of skull fracture Traumatic carotid-cavernous fistula (TCCF)
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www.RiTradiology.com 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
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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 www.RiTradiology.com
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SECONDARY LESIONS www.RiTradiology.com Herniation Cerebral edema Ischemia and infarction Secondary hemorrhage Hydrocephalus Brain death
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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 www.RiTradiology.com
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Herniation www.RiTradiology.com
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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 www.RiTradiology.com
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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) www.RiTradiology.com
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Herniation: Subfalcine and Midline Shift Measured at level of foramen of Monro Distal ACA may be compressed against falx www.RiTradiology.com
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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 www.RiTradiology.com
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Herniation: Descending Transtentorial Before surgery www.RiTradiology.com After surgery
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Herniation: Ascending Transtentorial Cranial shift of vermis and parts of superomedial cerebellar hemisphere through tentorium incisura Compressed superior cerebellar, vermian cisterns and forth ventricle www.RiTradiology.com
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Posttraumatic Cerebral Edema www.RiTradiology.com 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
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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 www.RiTradiology.com
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www.RiTradiology.com 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) At time of trauma 3 months later
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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 www.RiTradiology.com
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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 www.RiTradiology.com
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www.RiTradiology.com 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
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Conclusions www.RiTradiology.com 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
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Conclusions www.RiTradiology.com 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