Emergency Radiology Notes PDF

Emergency Radiology Neuro General notes Dxx of hemorrhagic masses ○ GBM ○ Pituitary macroadenoma ○ Hemorrhagic metastasis Melanoma RCC Thyroid cancer Choriocarcinoma Complications of the depres...

Emergency Radiology Neuro General notes Dxx of hemorrhagic masses ○ GBM ○ Pituitary macroadenoma ○ Hemorrhagic metastasis Melanoma RCC Thyroid cancer Choriocarcinoma Complications of the depressed skull fracture ○ Epidural abscess ○ Dural venous thrombosis, especially SSS Stroke Resources ○ 1. Imaging of Acute Hemorrhage and Ischemic Stroke.pptx (2021 Classic Lectures in Emergency and Urgent Care Radiology course) ○ 19. Stroke Imaging Update.pptx (2021 Classic Lectures in Emergency and Urgent Care Radiology course) Definition- a syndrome of acute neurological dysfunction d/2 ○ Ischemia ○ Intracerebral hemorrhage (IPH, IVH) ○ Subarachnoid hemorrhage ○ Venous thrombosis Clinical presentation ○ Sudden onset ○ Loss of function ○ Usually painless Infarction is brain, spinal cord or retinal cells death d/2 ischemia Silent stroke: infarction without attributable symptoms Types of stroke ○ Ischemic stroke Most common ~ 85% d/2 interruption of arterial supply (thromboembolic) ○ Hemorrhagic stroke (term falling out of favor) Intraparenchymal hemorrhage- most common Often d/2 hypertension 1  Subarachnoid hemorrhage- less common 85% of spontaneous SAH d/2 aneurysm rupture (remember, the most common cause for SAH is trama) ○ Transient ischemic attack (definition varies) “Mini-stroke” resolving within 1 hour (previously 24 hours) High risk for future stroke ⅓ will have major stroke within a year if not treated 10-15% will have major stroke within 3 months Hemorrhagic stroke (term is out of favor) Approach ○ Under 40-Y → 50% have underlying vascular malformation ⅔: AVM ⅓: cavernous malformation ○ Greater 70-Y Amyloid angiopathy HTN ○ 40 - 70 Up to 70% → hypertension ○ Multiple / bilateral → think of hemorrhagic venous infarct 4 types of non-traumatic intracranial hemorrhages ○ Subarachnoid hemorrhage ○ Intraventricular hemorrhage ○ Lobar intraparenchymal hemorrhage ○ Deep intraparenchymal hemorrhage Peripheral lobar intraparenchymal hemorrhage, think of; 1. CAA. 2. Hemorrhagic transformation of venous infarct. 3. Vascular malformation. Venous thrombosis can be presented with isolated SAH (cortical venous thrombosis) or lobar hemorrhage (sinus thrombosis) Intraparenchymal hemorrhage in patients with preexisting hypertension in typical locations (basal ganglia, thalamus, external capsule or posterior fossa) requires no further evaluation. However, lobar or deep brain bleeds in younger patients or normotensive adults—regardless of age—almost always require further investigation The presence of an intraventricular haematoma is considered a poor prognostic factor d/2 the obstruction to CSF with hydrocephalus and raised intracranial pressure. As a rule, intraparenchymal hemorrhage can spread into subarachnoid space, and the opposite is true when an aneurysm ruptures the pressure of the jet can be so high, that the blood will be injected into the brain parenchyma Spreading of hemorrhage along the falx (parafalcine) or tentorium (peritentorium) → not EDH. It is either; ○ SDH → no blood in sulci ○ SAH → a/w blood in sulci Non-traumatic subarachnoid hemorrhage Table for different etiologies 2  Causes of convexal SAH ○ RCVS ○ Cortical venous thrombosis Aneurysmal SAH ○ Account for 85% of spontaneous SAH (the most common cause) ○ DSA is the gold standard for diagnosis ○ Distribution may give hint of location Aneurysm SAH distribution ICA - PCoA aneurysm Suprasellar cistern Anterior communicating artery Septum pellucidum (in frontal lobes), interhemispheric fissure Middle cerebral artery Sylvian fissure (in temporal lobe) Anterior cerebral artery Sylvian fissure Basilar artery tip Interpeduncular fossa, brainstem or thalamus PICA 4th ventricle Vertebrobasilar aneurysms fourth ventricle, prepontine cistern and foramen magnum Non-aneurysmal perimesencephalic hemorrhage ○ 10-15 % of spontaneous SAH ○ Definition- on NECT within 3 days of symptoms onset Blood centered immediately anterior to midbrain or pons. It may extends into basilar cisterns, proximal Sylvian or interhemispheric but not in lateral portion of Sylvian fissure Small blood layering into the occipital horn of lateral ventricle, but no frank IVH or blood cast -ve CTA ○ Compared to BA tip aneurysm, this entity does NOT extends deep into Sylvian fissure, interhemispheric fissure or ambient cisterns Reversible cerebral vasoconstriction syndrome ○ Clinical: young middle-aged women with severe, recurrent headaches ○ Triggers Drugs (amphetamine, serotonergic antidepressant, nicotine, caffeine) Peripartum / eclampsia Strenuous physical activity Bathing / showering ○ Findings Convexal SAH Segmental vasoconstriction involving multiple vessels Abnormalities may develop in a delayed fashion (initial DSA is -ve) 3  Hallmark is resolution of vasoconstriction with supportive treatment and removal of trigger Cortical venous thrombosis ○ More, review here Notes of Radiology ○ Can be presented with isolated SAH (dural sinus thrombosis has more like lobar hemorrhage) ○ NECT shows hyperdense cord sign d/2 acute thrombosis ○ CECT shows filling defect in the cortical veins Non-traumatic intraventricular hemorrhage Differential diagnosis ○ 50% unknown / idiopathic ○ AVM ○ Aneurysm ○ Moya Moya ○ Dural AVM Complications ○ Obstructive hydrocephalus AVMs ○ Most common cause for ICH in patients < 40 Y ○ Peak age 20-40 Y Moya Moya disease ○ Definition- supraclinoid ICA occlusion ○ Vertebrobasilar system is usually spared ○ Etiology 1ry- very rare 2ry (Down syndrome, tuberous sclerosis, sickle cell anemia, atherosclerosis, radiation) ○ Imaging Puff of smoke vessels- they represent tortious lenticulostriate collaterals Deep intraparenchymal hemorrhage Dxx ○ Hypertensive hemorrhage ○ Cavernous malformation ○ AVM (especially in young) ○ Moyamoya Hypertensive hemorrhage ○ Classic location (central small perforating arterioles) Basal ganglia, thalamus, external capsule (75%) Pons, cerebellum (15%) 4  Centrum semiovale ○ Appropriate clinical history (hypertension) ○ Finding Deep microhemorrhages on T2* GRE confirmatory finding Extension into ventricular system is common (why) → b/c it is centrally close to the ventricles Cavernoma ○ Definition- blood filled hamartomatous venous malformation (immature vessels) ○ Location Random distribution (vs. central in hypertensive hemorrhage, and vs. peripheral in cerebral amyloid angiopathy) Supratentorial (60%) Infratentorial (40%) ○ Think cavernoma with hemorrhage if Small hematoma (< 3 cm) Calcifications Associated DVA ○ Imaging Classic finding: well-circumscribed mixed density / intensity mass surrounded by complete hemosiderin rim (popcorn ball) Multiple areas of hemosiderin deposition, different sizes Popcorn appearance, bright T1 & T2 appearance ○ Dxx of multiple microbleeds Diffuse axonal injury in trauma setting Hypertensive hemorrhage (central) Amyloid angiopathy (peripheral, old age) AVM Lobar intraparenchymal hemorrhage Dxx ○ Hypertensive hemorrhage ○ Amyloid angiopathy ○ Mass ○ Cavernoma ○ Hemorrhagic venous infarct ○ Metastasis ○ Drug-induced vasculitis (cocaine) Cerebral amyloid angiopathy ○ It is the diagnosis of exclusion, consider it in older patients ○ Usually associated with SAH → So if you see a lobar hemorrhage with some subarachnoid extension in an older person, you want to think about amyloid ○ Location 5  Peripheral (vs. random in cavernoma, deep in hypertensive hemorrhage) Isolated to cortical / subcortical junctions ○ Boston criteria The Boston criteria are dependent on pathology, and most patients are not willing to undergo brain biopsy. So radiology can help by making a diagnosis of probable or possible amyloid angiopathy Definite CCA- postmortem exam Probable with pathology Lobar / cortical or subcortical hemorrhage Path specimen with CCA Probable Multiple hemorrhages, restricted to lobar, cortical or cortical-subcortical regions Age > 55 Y No other causes of hemorrhage identified Possible Single lobar, cortical or cortical-subcortical hemorrhage Age > 55 Y No other cause of hemorrhage Hemorrhagic venous infarct ○ Also review: Notes of Radiology ○ Findings Unusual, weird / bilateral venous ICH Frontoparietal ICH (SSS thrombosis) Thalamic (deep venous / vein of Galen thrombosis) Isolated SAH (above) In cortical venous thrombosis Nonhemorrhagic infarction Vasogenic edema ○ Associated with OCPs Pregnancy / postpartum Sinus / mastoid infection Severe dehydration Hemorrhagic metastasis ○ Common hemorrhagic metastasis Breast & lung (most common) Melanoma, RCC, thyroid cancer, choriocarcinoma ○ Finding Usually multiple ○ GBM can hemorrhage Drug induced vasculitis (cocaine) ○ Presentation 6  Intraparenchymal hemorrhage SAH Ischemic stroke / TIA ○ Imaging Vasculitides and the vasculopathies are going to look similar on angiogram Areas of irregular narrowing or beading ○ ICH may be related to BP spikes after cocaine use ○ Vasculitis may be related to direct drug injury or from contaminants ○ Trigger drugs Cocaine Amphetamine Heroin Ischemic stroke Role of imaging in ischemic stroke ○ Ischemic stroke ○ Venous infarct Protocol ○ “Time is brain” → ER radiology in 30 minutes ○ Clear a CT scanner ○ STAT head CT Non-contrast CTA ○ Blood on head CT ? No → CTA of head & neck Yes → CTA of head only (why?): to optimize that contrast bolus and the field of view to get detailed evaluation of the blood vessels to look for aneurysms, small aneurysms, AVM… Imaging morphology ○ Cytotoxic edema → preferential gray matter CT → low density DWI → “light bulb”- most sensitive ○ Respects vascular territory (artery or vein) ○ Follows expected temporal evolution tPA candidate (what is important in radiology) ○ Inclusion criteria No blood on CT Extensive edema > ⅓ MCA territory (b/c there is risk of reperfusion hemorrhage) Time of last normal < 4.5 hours ○ Cautionary criteria Early brain ischemia on CT Known neoplasm (vasogenic edema), AVM, aneurysm Long clot length (? => 8 mm) 7  ○ Exclusion criteria CT confirms hemorrhage (IPH, SAH) Role of CT ○ Find alternative or unexpected diagnosis (b/c early infarct is often occult on CT) ○ Evaluate for imaging contraindications to giving tPA Intracranial hemorrhage Well-demarcated infarcts greater than ⅓ MCA territory CT finding ○ Tips Use stroke window Specifically evaluate Basal ganglia Insular ribbon 2nd look at areas based on clinical history (So if they have right-sided hemiparesis, you want to take a second look at the left side of the brain. If they have aphasia you want to take a second look at the left side of the brain) By contrast, the ischemic changes will be better depicted b/c the normal enhancing tissue is more denser Thin sections (1.25 mm) increase sensitivity for hyperdense MCA sign ○ Dense vessel sign It suggests acute MCA occlusion Associated with large territory infarct and poorer outcome ↑ attenuation of an acutely thrombosed vessel Attenuation of affected vessel should be greater than that of other vessels ○ Dense dot sign Smaller hyperdense focus in the Sylvian fissure Represents acute thrombosis of MCA branch ○ Dense basilar sign is difficult d/2 Calcified atherosclerotic plaque Beam hardening from the skull base bones No paired internal controul (unlike MCA) ○ Insular ribbon ○ Hypodense lentiform nucleus ASPECTS score ○ It ake a typical MCA distribution from the ganglionic level up to the top of the ventricles ○ ASPECTS 70 Hounsfield units is likely thrombosed ○ Or ratio of attenuation value to hematocrit → >1.5 concerning Can be presented with intracranial hemorrhage as ○ Isolated SAH in cortical venous thrombosis ○ Unusual ICH in sinus thrombosis Pearls ○ GRE may show hyperdense cord sign of thrombosed cortical vein Pitfalls ○ Deoxyhemoglobin is dark on T2 and this mimics flow void on T2, therefore T1 is the most important sequence Sagittal sinus thrombosis Imaging ○ Bilateral & multifocal d/2 involvement of a large sinus ○ CT NECT- hyperdense sinus, cord sign, congested meninges, hemorrhagic infarction CECT- empty delta sign; enhancing dura around non-enhancing thrombus ○ MRI T1 (most important)- bright blood in the SSS with loss of flow void T1+c- empty delta sign T2- less sensitive b/c deoxyhemoglobin is dark on T2 and mimics flow void DWI- restricted diffusion if infarction develops (usually does) GRE- blooming of the dural vein MRV- no flow Transverse sinus thrombosis Case studies: example 1| The most common dural sinus undergoes thrombosis Common etiologies 10  ○ Infection from mastoiditis, through the transosseous emissary veins, or scalp infection ○ Propagates from jugular venous thrombosis Differential consideration of small TS ○ Hypoplastic TS- is a normal variant 50% right dominant, 25% equal, 25% unilateral ○ Arachnoid granulation ○ Idiopathic intracranial hypertension Vein of Labbe ○ It is a cortical vein that drains into the TS ○ Thrombosis of the TS can leads to venous occlusion of vein of Galen → ischemia / hemorrhage of the posterior temporal lobe Deep Cerebral Vein thrombosis Compared to the dural venous thrombosis, it has high mortality Always bilateral → venous congestion / infarction of the basal ganglia & thalami Thrombus can be seen in the; thalamostriate, deep cerebral veins and straight sinus Common causes ○ Extension from dural sinus thrombosis ○ IF; ○ Hyperdense ICVs & straight sinuses ○ Bithalamic edema with effacement of the borders between the deep gray nuclei and internal capsule ○ Thalamic lacunar hemorrhage Differential diagnosis ○ Neoplasm (bithalamic glioma) ○ Wernicke encephalopathy Cavernous sinus thrombosis / thrombophlebitis Clinical manifestations ○ Retro-orbital pain with edema ○ Proptosis ○ Ecchymosis Special causes ○ Sinusitis, the most common cause (by staphylococcus aureus) ○ Meningitis ○ Local skin infection Pathology ○ CS has numerous valveless communication with the vein of the orbit, face & neck, so infection can spread through these conduits Imaging ○ Best modality → T1+c fat-sat ○ CT 11  NECT- lateral bulging of CS wall, thrombosed SOV, proptosis, “dirty” orbital fat, periorbital edema, sinusitis CECT- irregular filling defects within the expanded CS and SOVs ○ MRI Enlarged CV with convex lateral margins T1- isointense thrombus with loss of flow void T1+c fat-sat- nonenhancing filling defect within the enhancing dural wall Venous occlusion mimics / venous sinuses dynamics Intracranial hypertension ○ The venous sinuses, even though they're lined by dura, they're not as fixed and can get dilated / narrowed according to flow dynamics ○ So, intracranial hypertension the brain gets swollen and it actually squishes down (= narrowed) transverse sinus Intracranial hypotension ○ Other side of that coin, is if you have hypotension they can look very plump, but if you blood patch them, they go back down to normal so these can rise and fall depending on intracranial pressure dynamics Arterial occlusion Posterior circulation stroke Why is posterior circulation ischemic stroke difficult to diagnose? ○ Vague and non-specific symptoms ○ A lot of skull base bony artifacts ○ A lot of vascular variability especially PICA & AICA PCA density PCA can mimic the petroclinoid ligament. a/w PCA territory infarction. ICA density with occipital hypodensity Occurs in fetal origin of the PCA. Uncommon IF; ○ Hyperdense ICA in the carotid canal denoting occlusion. ○ Hypodensity and acute infarction of the occipital region d/2 fetal origin of the PCA. Basilar artery density Very rare. Usually patients don't make it to the ER. IF; ○ Hyperdense basilar artery ○ Hypodense pons denoting acute infarction Pitfalls 12  Hemorrhagic transformation of acute infarct ○ Occurs with extensive acute infarcts after attempted revascularization ○ Usually in the form of petechial hemorrhage not lobar ○ Location; basal ganglia & cerebral cortex (gyriform cortical) Pseudonormalization ○ It is a form of hemorrhagic transformation. ○ Occurs when there is bleeding in a non-salvageable compromised brain tissue → the dead tissue appears as normal brain (increased density d/2 blood). ○ It is a serious complication! Traumatic Brain Injuries Resources ○ 18. Head Trauma and Neurovascular Injury.pptx CT protocol of acute trauma ○ Begins with scout looking at the tubes and lines (how sick patient is) ○ Orbitofrontal & inferior temporal contusions best seen on 2D sagittal & coronals ○ High risk fracture should prompt CTA ○ IV contrast? Extravasation appears as spot sign (puddling of contrast in the center of the hematoma, could be dot or little collection) How is TBI classified? ○ Clinical severity- GCS, Amnesia, LOC (loss of consciousness) ○ Imaging severity- Rotterdam Score → radiological signs of bad prognosis Effacement / compression of basal cisterns Midline shift > 0,5 cm Associated SAH / IVH ○ Timing- primary Vs. secondary TBI ○ Mechanism- blunt, penetrating, blast ○ Location- intra-axial Vs. extra-axial Complications ○ Direct vascular disruption ○ Clot expansion → mass effect Local compression Herniation: uncal, subfalcine, downward ○ Edema Vasogenic: “benign” reactive edema Cytotoxic: 2ry ischemia d/2 Vascular compression (after herniation) Vasospasm (after SAH) ○ Hydrocephalus Communicating (intraventricular blood) Obstructive (mass effect) 13 EDH Etiology- develops when there is fracture through the calvarium, which can injury diploic veins or laceration of an artery Pathology- The blood will strip the outer periosteal layer of dura, and blood collect within the pocket It crosses the falx and tentorium and never cross sutures Low threshold for follow-up CT when: ○ Unable to properly examine ○ Clinical deterioration ○ Risky bleed ○ Risky fracture EDHs are not equal. Prognosis depends on ○ Location of hematoma Bad When hemorrhage occurs in the temporal area. It is near the uncus and can cause compression and effacement of basal cisterns (herniation) Not so bad- hemorrhage in the frontal area Better- EDH in the vertex, most likely venous origin (SSS injury) ○ Source of blood (arterial or venous) Bad- when the mechanism suggests arterial tear like squamous temporal bone fracture Benign- temporal epidural hematoma occurs d/2 injury to sphenoparietal sinus. So it is a venous pressure hematoma that's naturally limited by the temporal pole ○ Rapidity with which it collects Bad- “swirl sign” indicates an active bleed and hematoma appears heterogeneous SDH It will follow the dural reflections Posterior fossa collection are dangerous ○ It can develop herniation, compression of brainstem, closing off the 4th ventricle causing hydrocephalus 2 flavors of chronic SDH ○ Uncomplicated … evolving clot liquifies & becomes uniform near CSF density Managed by simple burr hole ○ Complicated … septations, fluid levels, blood of different ages Need craniotomy SAH SAH will follow the CSF spaces and tend to interdigitate like fingers down into sulci Check the dependent areas ○ Superior frontal sulcus ○ Posterior part of the Sylvian fissure ○ Base of the interhemispheric fissure ○ Interpeduncular cistern ○ Prepontine cistern. 14  ○ Fluid level at the base of the occipital horn of the lateral ventricles. ○ Cervicomedullary junction Diffuse Axonal Injury (= Shear Injury) Typical locations ○ Subcortical WM (usually in the frontal lobe) ○ Corpus callosum or septum pellucidum ○ Medial temporal cortex is always associated (Dr. Strong- vRad) IF ○ Dense rounded lesions not a/w surrounding edema Vs. brain contusion Pitfalls ○ Trauma → post op confusion? DAI or fat emboli? History is key Penetrating brain injuries Rule- as injury goes back to frontal lobes (or frontal horns of lateral ventricles), it will become more fatal Rule- non-ballistic penetrating TBI is better than ballistic penetrating TBI Traumatic cerebrovascular injury Importance- patients usually initially asymptomatic, so a high index of suspicion is necessary. Once symptomatic, the morbidity and mortality of these patients is high b/c they have either hemorrhage or infarction Findings of initial head and spine CT scans that suggest cerebrovascular injury ○ Any injury around the foramen magnum Atlantoaxial dissociation C1 / C2 fractures C-spine fractures crossing transverse foramen Central skull base crossing the carotid canal ○ Injury could be arterial or venous Classification of traumatic CVI ○ Raised intimal flap (dissection) ○ Intra- or extramural hematoma ○ Pseudoaneurysm ○ Occlusion ○ Rupture Hemorrhagic brain General notes ‫ﻻﺑد ﻣن ﺗﻔرﯾﻎ ھذا اﻟﻣﺣﺗوى ﻓﻲ اﻟﻘﺳم اﻟﺳﺎﺑق وﺣذف اﻟﻣﺗﻛرر‬ Unruptured basilar tip aneurysm can be presented with non-communicating obstructive hydrocephalus, if they are large enough to exert mass effect on brainstem and aqueduct. 15  ○ Remember, ruptured aneurysms can be complicated with obstructive hydrocephalus. (Don’t confuse the 2). ○ However, when finding an aneurysm, always keep looking for SAH. Non-traumatic intracranial hemorrhage (a.k.a. spontaneous) Read again; intracranial which includes intraaxial and extraaxial The extraaxial variety of concern in this context is; SAH, b/c EDH and SDH occur with trauma. Remember; the most common cause of SAH is trauma Classification ○ Intraparenchyma Feature- no underlying structural abnormality The most common causes; 1. Hypertension. 2. Cerebral amyloid angiopathy. Together they constitute 85% of all causes of non-traumatic hemorrhage Other causes: 1. Anticoagulant / coagulopathy. 2. Illicit drugs (e.g. cocaine). 3. Hemorrhagic venous infarcts. 4. AVM. 5. Aneurysm. 6. Metastasis. 7. Primary brain tumors (ependymoma, glioblastoma). 8. Hemorrhagic transformation of arterial infarcts ○ Subarachnoid The “spontaneous” SAH Causes: 1. Ruptured aneurysm. 2. Nonaneurysmal perimesencephalic SAH Frontal / parietal lobar hemorrhages can occur with; 1. CAA. 2. Vein of Trolard hemorrhagic venous infarct. Stages of intraparenchymal hematoma ○ Hematomas consist of: A central core and a peripheral rim. ○ In general, Hgb degradation begins in the clot periphery and progresses centrally toward the core. Pearls ○ Cerebral amyloid angiopathy Epidemiology- age > 65Y Pathogenesis- deposition of B-amyloid protein in the wall of blood vessel leading to weakness Location- peripheral; lobar (frontal, parietal), subcortical white matter Forms- ○ 1. Microbleeds. ○ 2. Macrobleeds ○ 3. Cortical superficial siderosis- cortical subarachnoid hemorrhages that follow the curvilinear shape of the surrounding cerebral gyri Usually it does not extend into the ventricular system (why?) → b/c it is peripherally located Imaging ○ MRI- to detect hemosiderin deposition resulting from microbleeds. It appears dark signal on gradient 16 Hemorrhagic Venous Infarcts Location of hemorrhage may give a clue of venous thrombosis ○ Vein of Labbe thrombosis Inferior anastomotic vein between the Sylvian vein and transverse sinus Infarction/hemorrhage typically occur in the; temporal lobe ○ Vein of Trolard Superior anastomotic vein between the Sulvian vein and superior sagittal sinus Infarction/hemorrhage typically occur in the; frontal or parietal lobe Imaging ○ Triangular hyperdense sign ○ Cord-like hyperdense sign Arteriovenous Malformation AVM has 3 components; 1. Feeding artery. 2. Nidus. 3. Draining veins Post-aneurysmal SAH complications ○ Cerebral ischemia and vasospasm → CTA/DSA; multiple segments of vascular constriction and irregularly narrowed vessels. ○ Obstructive hydrocephalus. ○ Rebleeding Convexal SAH ○ Definition- isolated spontaneous non-traumatic non-aneurysmal SAH over the brain vertex ○ Location- is characteristic; restricted to the hemispheric convexities, sparing the basal & perimesencephalic cistern ○ Common causes; < 60 → Reversible Cerebral Vasoconstriction Syndrome More in women Presents with frontal convexity SAH. > 60 → cerebral amyloid angiopathy All ages → vasculitis, venous occlusions SAH The traumatic and aneurysmal SAH has different patterns of distribution. The distribution of blood can hint at the expected location of the ruptured aneurysm. Look for hidden areas before concluding “there is not SAH” Traumatic SAH distribution ○ Anterior-inferior frontal lobe. ○ Temporal sulci. ○ Perisylvian regions. ○ Hemispheric convexities. ○ Look also for; adjacent brain contusions, EDH, SDH, skull fractures, skull base gas Dxx 17  ○ Perimesencephalic nonaneurysmal SAH The most common cause of non-traumatic non-aneurysmal SAH Location- subarachnoid blood in the; interpeduncular, ambient and prepontine cisterns. Suprasellar cistern is clear CTA; -ve for aneurysms. ○ Convexal SAH Definition- isolated spontaneous non-traumatic non-aneurysmal SAH over the brain vertex Location- is characteristic; restricted to the hemispheric convexities, sparing the basal & perimesencephalic cistern Common causes; < 60 → Reversible Cerebral Vasoconstriction Syndrome ○ More in women ○ Presents with frontal convexity SAH. > 60 → cerebral amyloid angiopathy All ages → vasculitis, venous occlusions ○ Pseudo-SAH In severe brain edema like in; meningitis, post-cardiac arrest, brain death, anoxic injury ○ Dural AV fistula It can mimic SAH in both symptoms and imaging presentation. It has both SAH and parenchymal hemorrhage. ○ AVM It may be presented as SAH. Syndromes a/w vascular aneurysms ○ ADPKD ○ FMD ○ Persistent trigeminal artery Aneurysms Unruptured BA aneurysm (= tip aneurysm) ○ Imaging Well-delineated midline mass with peripheral mural calcification Obstructive hydrocephalus (unusual presentation); if they are large and exerts mass effect on brainstem and aqueduct → non-communicating hydrocephalus No SAH Unruptured CPA aneurysm ○ Imaging Well-defined hyperdense mass on CPA ○ Dxx Meningioma Schwannoma SDH Common among elderly (brain atrophy is susceptible to velocity injury) 18  Like SAH, the most common cause; trauma Most common location; supratentorial Common a/w mass effect in the form of; subfalcine herniation Prognosis depends on ○ Hematoma thickness ○ Midline shift ○ Associated parenchymal injuries Forms ○ The classic; supratentorial crescent shape extraaxial collection ○ Parafalcine ○ Peritentorium Causes of isodense aSDH ○ Extremely anemic patient ○ Patient with anticoagulation ○ Associated CSF leak through torn arachnoid layer ○ How to detect this subtle hemorrhage? Mass effect in the form of midline shift. The hypodense white matter doesn;t reach the end (compare to other side) Effacement of the sulci adjacent to the bone ((compare to other side) Dxx ○ EDH Biconvex Vs. crescent shape in aSDH Always a/w skull fracture Vs. aSDH occurs with absent fracture Cross the dural attachment Vs. aSDH never cross falx or tentorium Never cross the sutures Vs. aSDH can cross the sutures Pearls ○ Unlike EDH, only small amount of SDH can be a/w massive effect. Thus, if the distinction between EDH / SDH is unclear, look for mass effect / midline shift, common with SDH. ○ Epidural hematoma is usually not a/w mass effect, b/c of contained blood. The exception is the EDH in the posterior cranial fossa. BRAIN CONTUSIONS Occur in highly predictable locations ○ Anterior inferior (orbital) surfaces of the frontal lobes (just like tSAH) ○ The temporal poles ○ Perisylvian gyri (just like tSAH) IF; ○ Focal areas of petechial hemorrhage, surrounded by hypodense areas of edema DURET HEMORRHAGE Location; centrally located in the midbrain a/w; transtentorial herniation → compromise of brainstem circulation → infarction & hemorrhage 19 Vasculopathies MOYA-MOYA DISEASE Common among asians (korea/japan) IF; ○ Marked narrowing of both supraclinoid ICAs, which results in ○ Extensive BG and WM collaterals (puff of smoke sign) ○ Acute parenchymal hypertensive hemorrhage Brain tumors in the ED Resources ○ 20. Brain Tumors in the ED - Pearls _ Pitfalls (University of Washington Emergency Radiology Review 2023) ○ Emergency Imaging of Brain Tumors: Introduction/Role of Imaging Subtle signs of brain tumor in the CT ○ Cortical / structural expansion Cortical based primary brain tumors tend to expand the cerebral gyri Increase cellularity usual results in structural expansion or mass effect History: seizure, headache, sensory changes, lack of trauma, etc ○ Hypoattenuation and mass effect Patchy white matter hypoattenuation is commonly present on CT Head. Especially in the periventricular and subcortical regions. Lacks mass effect is important criteria to differentiate “benign” hypoattenuation from that of underlying lesion Difficult to differentiate simple edema vs tumor infiltration Mass effect signs Effacement / compression of the adjacent ventricle ○ Hemorrhage The lesion can be either hemorrhagic mets or angioinvasive 1ry brain tumors Hemorrhagic mets- melanoma, RCC, thyroid cancer, choriocarcinoma Angioinvasive tumor- glioblastoma ○ Extra-axial tumor signs Expansion of the IAC in CPA-angle tumors, especially acoustic neuroma (schwannoma) Bony hyperostosis in meningioma Sellar expansion in pituitary macroadenoma ○ Calcification occurs with Meningioma Oligodendroglioma Pitfalls ○ Brain infarct 1ry brain tumor can involve the gray matter, mimicking infarct 20  The infarct usually involves both white & gray matter, while 1ry tumors usually involve the white matter Acute spine emergencies Resources ○ 7. Non-traumatic Spinal Emergencies.pptx Entities ○ Back pain ○ Neck pain ○ Infection ○ Vascular lesions and mishaps ○ Inflammatory conditions ○ Masses / neoplasms Who to image? ○ Imaging of low back pain is generally not recommended if there are no red flags ○ Radiculopathy It is shooting pain down to the extremity Most acute radiculopathies improve with conservative care, thus awaiting 6 weeks prior to imaging is preferable Many acutely herniated disc ○ Red flags Trauma Unexplained weight loss Age > 50-Y especially females, or males with osteoporosis or compression fracture Unexplained fever, H/O infection Neurocompression, diabetes IVDA Prolonged corticosteroid use, osteoporosis Age > 70-Y Focal neurological deficits with progressive or disabling symptoms, especially cauda equina syndrome Duration > 6 weeks Prior surgery Back pain Cauda equina syndrome ○ It is a true neurosurgical emergency and it differs from acute radiculopathy ○ Symptoms- saddle anesthesia, bladder dysfunction, severe / progressive weakness or sensory deficits in lower extremities Disk herniation Acute neck pain Like low back pain, many cases resolve within 6 weeks 21  Red flags to image ○ Trauma ○ Rheumatoid arthritis (risk of atlantoaxial subluxation) ○ Fever, weight loss ○ Upper motor neuron signs (myelopathy) ○ Age < 20 or > 60 ○ Associated chest pain or signs of MI ○ Stroke symptoms (carotid or vertebral artery dissection) Central cord syndrome ○ Etiology- trauma, hyperextension injury ○ clinical ly- upper >> lower extremity weakness; bladder dysfunction; variable sensory loss ○ Imaging features Central canal stenosis ↑ T2/STIR signal within the cord Infection Definition- inflammation of the vertebral body (osteomyelitis) and disc (discitis), and together are known as; infectious spondylitis Forms of spinal infection ○ Discitis / osteomyelitis ○ Facet septic arthritis ○ Epidural abscess ○ Rules ○ The normal epidural space, the enhancement of the epidural space has mustache-look to it which is a classic appearance of a normal epidural venous plexus, so no epidural extension here and no compression of the thecal sac Importance ○ It often goes undiagnosed or diagnosed late with significant morbidity and mortality (why?) No classic history or findings Delayed diagnosis by 11 - 59 days ○ Spine lies in close proximity to: aorta, spinal cord and mediastinum ○ In reporting comment on Level Disc involvement Pathological fracture Epidural component Cord compression Soft tissue abscess: retropharyngeal, psoas Facets Post treatment ○ Imaging findings lag behind clinical 4-8 weeks ○ Signs of recovery or successful treatment Earliest- decrease in soft tissue component Reconstitution of fatty marrow 22  Epidemiology- males > 50-Y Risk factors ○ DM (the most common) ○ Risk factors for bacteremia: 1. IVDA 2. Indwelling catheters ○ Immunocompromised Pathogenesis ○ Pyogenic infections A nidus of infection which is hematogenous —> goes to the vascular part of the vertebral body, commonly along the posterior margin where the venous plexus comes in —> the infection is able to spread to the disc, which is relatively avascular, and provides a nice nutrient-rich environment that is low host-defenses —> rapid spread across the disc —> becomes a paraspinal infection and can extend into an epidural space —> epidural abscess ○ Granulomatous infections Instead of the centered within the disc and spreading to the bones, the discs often spared early and that is b/c organisms, in granulomatous spondylodiscitis, lack the protease enzyme to enter the disc and infect it So, in granulomatous spondylodiscitis, which is mostly TB, there is “subligamentous spread”, notice also the “skip lesions” as the infection spread sub-ligamentously to other regions of the spine Classification of spinal infections ○ Types Pyogenic spondylodiscitis (= suppurative) Location- lumbar spine Route of spread ○ Hematogenous (GU, skin, respiratory tract infections) ○ Transvenous (UTI, pelvic infections) via plexus of Batson ○ Direct (surgery, intervention as in pain injections) Causative organisms ○ Staph.aureus > 50% (MRSA is 40% of these) ○ Polymicrobial ~ 10% Granulomatous spondylodiscitis (= TB variety) Route of spread- hematogenous It begins in the subchondral bone adjacent to the endplate It extends in the subligamentous part of the ALL (skip lesions) Discs are spared early Fungi Nocardia Coccidiomycosis ○ Routes Hematogenous spread Staph.aureus E.coli ○ Occurs commonly in the: lumbar spine Direct inoculation 23  Surgery Trauma ○ Fractures serve as a nidus for infection Soft tissue infection ○ Extension of infection from retropharyngeal soft tissue into the spine Mixed organisms Opponostic infections TB Brucellosis Fungal ○ Coccidioidomycosis 10% of disseminated organism is in the spine ○ Location within the spine Hematogenous Vertebral body Spread to avascular disc Facet joint Facet joint is a true synovial joint with blood supply, thus can serve as a nidus for infection → facet septic arthritis Venous plexus Lumbar ○ The lumbar spine has a “Batson venous plexus” which is a connection between the bladder and the distal urinary tract , this same plexus drains the lumbar spine, so there is ability of the bacteria to go back and forth to the bladder and the spine —> so there is hematogenous, but venous extension from the UTI to the lumbar spine Direct inoculation Surgery Trauma Skin infection ○ Indications of surgery Neurological deficit bowel/bladder dysfunction (cauda equina syndrome) Weakness Sepsis Deformity Instability Collapse > 50% >20 degree angulation >5 degree translation Failed medical management Imaging of discitis / osteomyelitis ○ Radiograph Endplates irregularity & destruction (the best sign) Disc space narrowing 24  Acute angulation of the spine Paraspinal soft tissue swelling ○ CT Low-attenuation paraspinal swelling & edema Focal fluid collection Fat stranding Gas Enhancement of actively inflamed tissue with central nonenhancing area representing abscess Acute / early / active infection Subchondral erosion (endplates destruction) Demineralization, erosion & destruction of the in the cortex or endplates Soft tissue calcification in TB Abscess formation or extension into epidural or paravertebral spaces ○ CECT: non-enhancing low-attenuation central debris surrounded by a thick rim of ill-defined margins Chronic Sclerosis of the bones involved Deformity and collapse ○ MRI The most sensitive modality T1 Loss of marrow signal Loss of the black cortical line Loss of disc space height (= disc space narrowing) or pathological fracture Pre/paravertebral soft tissue edema, abscess Epidural phlegmon, abscess T1+c: ○ Enhancing disc and marrow ○ Enhancing soft tissue surrounding central non-enhancing component representing an abscess T2 Disc: 1. Hyperintense 2. Loss of intranuclear cleft (normally hyperintense) Edema of the vertebral body (T2-fat-sat) Spinal cord compression with effacement of the surrounding CSF DWI Abscess portion of discitis/osteomyelitis will demonstrate restricted diffusion Granulomatous discitis / osteomyelitis ○ The classic form is: TB (Pott’s disease) ○ Risk factor- immunocompromised ○ Location- the most common location is TL junction ○ Features of TB discitis / osteomyelitis Multiple levels / skip lesions (noncontiguous) Chronic / insidious Soft tissue component 25  Tracking under the ALL It spares the discs ○ Imaging The vertebral disk is relatively spared compared to the pyogenic spondylodiscitis Large paraspinal abscesses Bone destruction Other forms of discitis / osteomyelitis ○ Coccidioidomycosis Permeative or punched-out lesions Discs are spared (like other granulomatous entities) Preserved vertebral body morphology Not disc centered No disc erosion ○ Brucellosis Zoonotics: GI, respiratory or abrasions in diary workers Post-intervention discitis / osteomyelitis ○ Route of infection: by direct skin flora ○ Causative organisms: 1. Staph.aureus 2. Staph.epidermidis ○ Characteristic feature: raising CRP 96 hours post-op ○ Normal postoperative findings T2 hyperintense disc Linear disc enhancement Nerve root enhancement ○ Abnormal findings Enhancing paravertebral or epidural soft tissue Loss of the subchondral endplate definition, erosions and destruction Facet septic arthritis ○ Epidemiology- 4 - 20% of spine infections ○ Route of spread- hematogenous > iatrogenic ○ Presentes more acutely compared to the discitis / osteomyelitis ○ CT shows features of septic joint; Widening of the disc space Loss of bone on both sides Erosion of the subchondral bone ○ MRI T1 Loss of marrow signal T1+c: enhancing soft tissue surrounding that facet joint T2 Increased T2 signal ○ Dxx Degenerative facet disease 26  Complications of spine infections ○ Paravertebral / retropharyngeal abscess ○ Epidural abscess Clinical symptoms Para- or quadriplegia d/2 cord compression Neural deficit occurs d/2: arterial occlusion, venous thrombosis or vasculitis Imaging features Rim enhancing collection Central T2 hyperintensity ○ Mycotic aortic aneurysm Mimickers ○ Type 1 endplate changes Endplates enhance Marrow edema Usually defined Vs. infection: diffuse edema Transition Vacuum disc T2 hypointense disc Claw sign: well-defined border response between vascularized and normal marrow Psoas sign: T2 hyperintense psoas is highly specific for infection ○ Dialysis-related spondyloarthropathy Location- C-spine then lumbar Unlike discitis, there is low T2 signal of the disc d/2 amyloid deposition and no edema ○ Spinal neuropathy It is disc centered process with progressive destruction in setting of diminished sensation Characterized by 5 Ds Dense (sclerosis) Degeneration Destruction Deformity Debris T2 hypointense disc, unlike discitis with proliferic bone formation ○ Acute Schmorl node Acute can be symptomatic Usually involves multiple levels vs. spondylitis Marrow edema and enhancement Well-defined concentric hyperintense T2 ring 1 endplate, no other disc involvement 27  ○ Calcific tendonitis Longus colli Example 1| example 2| Definition- atraumatic inflammatory / granulomatous response to calcium hydroxyapatite crystals deposition in the longus colli tendons Clinically triad of: fever, dysphagia, neck pain Location - the superior oblique portion at the C1-C2 level Elevated CRP, WBC Imaging Amorphous calcification anterior to cervical spine (usually C1 / C2). No rim of sclerosis to suggest ossification that occurs with degenerative disease (osteoarthrosis) Asymmetry of longus colli muscle Minimal marginal enhancement of effusion in retropharyngeal space (retropharyngeal effusion) No bone destruction ○ rhBMP Endplate osteolysis in 100% cervical spine, 80% lumbar in 6 weeks Dose dependent Comparison, look here also Pyogenic spondylodiscitis Granulomatous spondylodiscitis Brucellosis Coccidioidomycosis Onset Acute (days to months) Indolent (months to years) H/O exposure Can resemble TB, mets Symptoms Sharp pain, spiking fever Dull pain, low-grade fever, night sweats Risk factors DM, IVDA HIV, endemia Markers Elevated ESR, CRP, WBC Elevated to a lesser degree Structure affected primarily Disc destruction Osseous destruction Vertebral bodies Disc T2 hyperintense, enhancing, Often spared until late disease Spared ‫ب‬ abscess Vertebral body enhancement Homogenous, diffuse Heterogenous, focal (patchy) Intraosseous abscess Rare Common Deformity Local kyphosis Greater degree of kyphosis, Vertebral body morphology Lytic or punched-out lesions Gibbus deformity maintained Paraspinous soft tissue Ill-defined enhancement Abscess with well-defined margins Loculated abscess Calcifications Location Lumbar Thoracic Lower lumbar spine 28 Spinal cord infarct Etiology ○ Atherosclerosis ○ Thoracoabdominal aneurysm ○ Aortic surgery ○ Systemic hypotension ○ Dissection ○ Coagulopathy Imaging features ○ Slightly expanded cord ○ ↑ T2/STIR central signal ○ Axial- gray matter involved ○ MRA- not helpful as ASA is too small to image Spinal cord hemorrhage Dxx ○ Dural AVF / malformation ○ Cavernous malformation ○ Hemorrhagic mass lesion: hemangioblastoma ○ Rarely, spontaneous Imaging features ○ Low T1 / low T2 indicating hemorrhage ○ Cord edema throughout the spine ○ No enhancing lesion ○ Spinal angiogram is -ve Dural AVF Imaging features ○ Enlarged edematous cord ○ Prominent flow voids on the cord surface ○ Vessels enhance ○ Spinal angiogram is gold standard for diagnosis ○ Endovascular treatment is common Cavernous malformation Review here Transverse myelitis Location- thoracic more common 29  Etiology ○ Idiopathic Likely undetected viral ○ Secondary (= transverse myelopathy) Autoimmune- SLE, Sjogren, sarcoidosis, mixed connective tissue disease Viral- EBV, CMV, HZV, HIV, enterovirus Other infection- syphilis, Lyme, mycoplasma, schistosomiasis Post-vaccination immune response Post-irradiation Paraneoplastic syndrome- lung, breast, HCC, MM, lymphoma, leukemia Imaging features ○ Cord lesion > 2 vertebral segment long ○ ⅔ axial area of cord affected ○ Cord expansion ○ Variable enhancement Dxx ○ Multiple sclerosis- < 2 vertebral segment involved ○ Neoplasm- heterogeneous, edematous, cystic +/- hemorrhage, slow symptom onset ○ Cord infarct ○ Neuromyelitis Optica ○ ADEM Dxx of multiple T2 hyperintense lesions of the cord Demyelination ○ MS Oval, peripheral and asymmetric lesions Usually discrete Affect gray & white matter May enhance if acute / subacute Later stage: cord atrophy With brain lesions → it is MS ○ Neuromyelitis Optica (= Devic disease) Definition- it is autoimmune inflammatory disease Isolated spine and optic nerve involvement Long lesions > 3 segments ○ ADEM ○ NMO Transverse myelitis Intramedullary tumor (sclerotic mets) ○ 1ry, also refer to spine neoplasms Myxopapillary ependymoma (intramedullary) Most common 1ry spinal cord tumor in adults Location- cauda equina, conus, filum Features 30  ○ Intensely enhancing mass within the distal cord Meningioma (intradural extramedullary) Features ○ Prominent enhancement ○ Dural tail Schwannoma Location- thoracic Features ○ Dumbbell shape as it exits the foramen ○ Intense enhancement ○ May be cystic or hemorrhagic Leptomeningeal carcinomatosis Definition- nodular enhancement along the spinal cord and nerve roots Metastatic disease- breast, lung, melanoma, lymphoma 1ry CNS tumors- GBM, medulloblastoma, PNET, ependymoma (not myxopapillary), germinoma, choroid plexus carcinoma ○ Sclerotic mets Location- posterior vertebral body > pedicle (Vs. spondylodiscitis) Common source- prostate, RCC, breast, lung Imaging features ↓ T1 / ↑ T2 & STIR Bone enhancement Spares disk (VS. pyogenic spondylodiscitis) Draped curtain appearance (indicative of epidural extension) ○ Osteolytic mets Common source- paraganglioma ○ Findings suggestive of metastasis with fracture rather than benign fracture Complete marrow replacement Convex bulge of posterior border Pedicle involvement Epidural mass No band-like low signal in T1 Lack of vacuum cleft Miscellaneous RUPTURED DERMOID CYST IF; ○ Well-defined hypodense midline mass usually in the suprasellar cistern (usually) ○ Multiple fatty “droplets” disseminated in the CSF cisterns; suprasellar, interhemispheric fissure and sulci Rupture causes symptoms of chemical meningitis with seizure, headache, coma, vasospasm or infarction COLLOID CYST WITH OBSTRUCTIVE HYDROCEPHALUS 31  IF ○ A well-defined hyperdense mass wedged on the top of 3rd ventricle at the foramen of Monro. ○ Hydrocephalus SAH WITH VASOSPASM It is a complication of SAH IF ○ SAH with / without aneurysm. ○ Multiple cortical hypodensities scattered sporadically throughout the brain denoting acute infarction d/2 vasospasm. ○ Maybe a/w intraventricular hemorrhage and hydrocephalus Non-Traumatic Head & Neck emergencies Resources ○ University of Washington Emergency Radiology Review 2023 Classification ○ Eye ○ Sinonasal cavity ○ Oral cavity & pharynx ○ Temporal bone ○ Neck Orbit Orbital cellulitis ○ Preseptal Vs. postseptal ○ Orbital septum Thin sheet of fibrous tissue extends from the orbital rim periosteum to the tarsal plates of the eyelids (they are cartilaginous structures formed in the middle of upper and lower eyelids) ○ Predisposing factors- sinusitis (esp. ethmoid) ○ Complications (esp. With postseptal cellulitis) Visual loss Thrombophlebitis with extension into cavernous sinus, SS or IJV Intracranial spread Subperiosteal abscess ○ Imaging Underlying sinus disease (esp. ethmoid) Myositis (esp. postseptal)- enlarged heterogeneous muscles Engorgement of ophthalmic veins due to congestion Acute dacryocystitis ○ Definition- it is inflammation of acute lacrimal apparatus ○ Predisposing factor- stenosis or obstruction of nasolacrimal duct (congenital vs acquired) ○ Imaging 32