Neuro-imaging in Emergency Conditions

For educational purposes only

Neuro-imaging ��in Emergency Conditions

Rathachai Kaewlai, MD Division of Emergency Radiology Department of Radiology, Ramathibodi Hospital, Bangkok Annual Scientific Meeting of the Neurological Society of Thailand 15 Nov 2015, Dor-shada Resort by the Sea, Chonburi

Ramathibodi Emergency Radiology


Outline

CT vs. MRI for brain disorders

Radiation and IV contrast issues Systematic interpretation of emergency brain CT Cases demonstrating pearls and pitfalls in interpretation


Neuro CT vs. MRI

It’s like comparing a phone camera and an SLR

Inexpensive, fast, convenient Expensive, slow, inconvenient

but clearer pictures


CT: Pros and Cons

Good for “serious, life-threatening” problems

Good for hemorrhage and bones Good “enough” Clinically relevant findings in most emergent situations

Cons: Diseases in early stages, non-hemorrhagic lesions

Radiation exposure Contrast: Acute kidney injury, hypersensitivity


CT Radiation Exposure

Medical radiation IS a major source of radiation exposure in human – NCRP#160 (year 2009; National Council on Radiation Protection & Measurements)

37%

36%

12% 2% 0%

5% 3% 5%

Medical procedures

Natural sources


CT Radiation Exposure

Medical radiation errors are EXPOSED – more public attention


Tissue Sensitivity

Most sensitive

Least sensitive

Bone marrow (red), colon, lung, stomach, breast, lens Gonads Bladder, esophagus, liver, thyroid Bone surface, brain, salivary glands, skin

Ref: ICRP 2007

Tissue Sensitivity !  ~ rate of cell proliferation !  Inversely ~ to age !  Inversely ~ to degree of cell

differentiation !  Higher dose = more damage !  Young = more damage


Diagnostic x-ray Risk Procedures Effective Dose

(mSv) Risks

CXR (PA), extremity XR <0.1 Negligible

Abdomen XR, LS spine XR 0.1-1 Extremely low “death from flying 7200 km”

Brain CT, single-phase abdomen CT

(1-3) 1-10

Very low “death from driving 3200 km”

Multiphase CT 10-100 Low

Interventions, repeated CT >100 Moderate


What You Can Do

Be aware of radiation risk from CT

Use the right test with the right indication Be specific when requesting studies Ensure your radiologists have focused protocols for

specific indication, age and patient size Check estimated dose of your patients


Checking Estimated CT Doses of Your Patients

CT Dose Report (last series on PACS)

Generally acceptable standard CTDIvol <75 DLP <1000 per phase


Ramathibodi ER Experience Prior to

2011 2012 –

present Median dose

reduction P value

CTDIvol 109 52 -53% <0.01

Total DLP 2232 943 -57% <0.01

Effective dose 4.7 2.0 -57% <0.01

Sulagaesuan C, et al. J Med Imaging Radiat Oncol 2015 in press

Generally acceptable standard CTDIvol <75 DLP <1000 per phase Ref: ACR, European Commission

Rama ER (now)

Rama ER (2011)


Neuro CT with IV Contrast

Quite common, sometimes emergently needed

Should we wait for serum creatinine before administering IV contrast???

Suggested indications for obtaining creatinine before contrast Age older than 60 years History of kidney disease as an adult,

including tumor and transplant Family history of kidney failure Diabetes Rx with insulin or other

medications

Hypertension Paraproteinemia syndromes or diseases Current use of nephrotoxic medications


How Much Should We Concern?

Post-contrast acute kidney injury (PC-AKI) “correlative diagnosis” Creatinine change in 48 hours (due to various etiologies) after CM use

Contrast-induced nephropathy (CIN) “causative diagnosis” AKI secondary to contrast, subset of PC-AKI Rare occurrence


Contrast-induced Nephropathy��Controversies

Lack of clear definition of AKI

Lack of clear risk thresholds Serum Cr vs. eGFR? Old data from intra-arterial

(not intravenous) injection No control group in most

published literature

Unclear acceptable interval btw baseline renal function and IV contrast use


Acute Kidney Injury ��from IV Contrast

Frequency and magnitude of sCr change was similar in patients receiving contrast and those not receiving it

>50% of 30,000 patients having non-contrast CT showed change in sCr

>40% showed change of at least 0.4 mg/dL

Newhouse JH, et al. AJR Am J Roentgenol 2008;191:376-382.


IV Contrast: ??? Cause of AKI, Dialysis or Mortality

21346 patients undergone CT, half received IV contrast 1:1 matched on propensity score yielding similar demographics and comorbidities

Radiology December 2014


IV Contrast in Stroke Patients Without Knowing sCr: Is It Safe? Several reports in both ischemic/hemorrhagic stroke

patients indicate very low incidence of CIN Oleinik A, et al. Stroke 2009;40:2393

Study with control group, 539 patients No increased rate of CIN with CTA CIN found in 6% of CTA group, 10% of no CTA group “Hospital-acquired nephropathy” ~8%


Brief Approach to CT Interpretation

Clinical question first ! look for pathology suspected

Then ! systematic review of images Blood Can Be Very Bad

Check blind spots: sella, skull base, orbits, upper C


Reading Emergency Brain CT:��“Blood Can Be Very Bad” Blood Evaluate for hemorrhage (bright white on CT)

Blood isodense around 1-2 weeks Hypodense by 2-3 weeks EDH, SDH, IPH, IVH, SAH and extracranial hemorrhage

Cisterns Four key cisterns examined for blood, asymmetry and effacement: •  Perimesencephalic •  Suprasellar •  Quadrigeminal plate •  Sylvian

Brain Look for symmetry, gray-white differentiation, shifting, hyper- or hypodensity

Ventricles Hydrocephalus (first evident in dilation of temporal horns) Compression/shift of ventricular system

Bone Fractures increase suspicion for intracranial injury

Perron AD. Emergency Medicine. Philadelphia, London: Saunders; 2008


Brief Approach to CT Interpretation

Anatomical localization Intra- vs. extra-axial Extra-axial: skull/scalp/dura, subarachnoid, ventricles

Intra-axial: grey, white, or both

Vessels

Lesion characterization Density Pattern of edema Contrast enhancement

Mass effect


BLOOD

Evaluate for hemorrhage (bright white on CT) Blood isodense around 1-2 weeks

Hypodense by 2-3 weeks

EDH, SDH, IPH, IVH, SAH and extracranial hemorrhage


Blood on CT

Shades of gray

Air Fat CSF WM GM CM Bone Metal -1000 0 1000 HU

Description relative to gray matter (GM) CT attenuation of blood products depends on location,

mixture (i.e., with CSF), initial hematocrit and time from onset of bleeding


Hematocrit Effect

35-45 HU

Whole blood = cells + plasma

55-65% Plasma

Erythrocytes 35-45%

Leukocytes And platelets

0-10 HU

60-90 HU


Hypertensive Hemorrhage

50% of primary non-traumatic ICH

Elderly with systemic HTN

Predilection for areas supplied by penetrating branches of MCA and basilar arteries

Putamen and ext capsule 60-65%

Thalamus 15-20% Pons, cerebellum10% Lobar 5-15%

Hypertensive hemorrhage of the right putamen with mild surrounding edema


Hypertensive Hemorrhage

Neurologic deterioration common within 48 hr

Recurrent in 5-10% of cases usually in different location

80% mortality in massive ICH with IVH

Hypertensive hemorrhage in the left thalamus and posterior limb of the left

internal capsule


CTA Spot Sign

Suggesting hematoma expansion

Findings Appearance Serpiginous

Spot-like

Location Within margin of IPH No connection to outside vessel

Size >1.5 mm diameter in maximal axial dimension

Density At least double the density (HU) compared to background hematoma

Lesion number Multiple Single

Thompson AL, Kosior JC, Gladstone DJ, et al. Can J Neurol 2009; 36:456.

*


CTA Spot Sign

Prevalence of spot sign in primary ICH 13-32%

Predicting hematoma expansion (%) Sensitivity 38-93 Specificity 50-93

PPV 22-77

NPV 78-98 Accuracy 56-90

PLR 1.86-10.99 NLR 0.30-0.73

Giudice AD, et al. Cerebrovasc Dis 2014;37: 268

75%


“CTA spot sign”

1 day – expanding hematoma 2 days later – craniectomy performed

CTA Post

*

* *


CTA Spot Sign: Imaging Marker

Hematoma expansion

Active bleeding during surgery Postoperative rebleeding In-hospital death

90-day mortality

May help selecting patients with pICH for specific therapy (medical, surgical hemostasis)

Brouwers HB, et al. Neurology 2014;83: 883 Brouwers HB, et al. Stroke 2015;46: 2498


Lobar Hemorrhage: DDx

Vascular malformation, aneurysm

Tumor Amyloid angiopathy Hemorrhagic venous infarct

Hemorrhagic transformation of ischemic infarct

Hypertensive hemorrhage


* *

Lobar hemorrhage due to amyloid angiopathy Large lobar hemorrhage of the left temporal lobe without abnormal vessels or

enhancement. Susceptibility MRI showing several other microhemorrhages

Normotensive demented patient with lobar hemorrhage of different stages

*


Multicompartmental Hemorrhages: DDx

Trauma Coagulopathy

SAH-IVH Extension of large parenchymal hematoma to other spaces

Coagulopathic ICH: IVH, IPH and SAH


Nontraumatic ICH: ��Workup Scheme IPH – Classic hypertensive ! No further W/U

IPH – Lobar ! administer IV contrast (CTA, CTV or post-contrast CT) or MRI/MRA

SAH – CTA to rule out aneurysm rupture SDH, EDH – think trauma first Multicompartment – check coag profile


What Else May Appear Similar To Acute Blood on CT?

Pus (i.e., in subarachnoid space, ventricles)

Dense, packed cells

Faint calcification Administered contrast

Post intra-arterial thrombolysis – contrast leakage Differentiation from hemorrhagic transformation of infarct is difficult on first day. In general, contrast leakage decreases attenuation over time


CT Hyperdensity: ��Blood or Other Things? Differentiation relies on clinical setting, presence of

surrounding edema, Hct effect, comparison with previous studies

New CT technology may be helpful (dual-energy CT)


CISTERNS

Suprasellar Sylvian

Perimesencephalic

Quadrigeminal *Median, unpaired cisterns

Quadrigeminal*

Lamina terminalis cistern*

Interpeduncular cistern

Sylvian cistern

Crural cistern

Perimesencephalic

Suprasellar*

Sylvian


Subarachnoid Hemorrhage: Nontraumatic

Ruptured right PcoA aneurysm with SAH 80% of non-traumatic SAH is due to ruptured aneurysm

Commonly cisternal/deep SAH


* *

Ruptured right MCA aneurysm with SAH NCCT is 98-100% sensitive during the first 12 hours of onset.

Sensitivity drops to 93% at 24 hours, 57-85% at 6 days after onset


Nonaneurysmal perimesencephalic SAH 10% of nontraumatic SAH. Small amount, limited to interpeduncular cistern.

Presumed venous etiology with low recurrence

Images ©Neuroradiology on the Net @blogspot

The other 10% of SAH etiologies: brain AVM, spinal AVM, DAVF, venous infarct, tumor


CT-negative, then?

LP more sensitive than CT Negative NCCT but still suspicious of SAH – still need LP (MRI is problematic at perimesencephalic cistern due to

CSF flow artifact)

Medscape.com


“Cortical” SAH: DDx

Trauma, trauma, trauma

Rupture of distal aneurysm

Venous sinus thrombosis Reversible cerebral

vasoconstriction syndrome (RCVS)

Cortical SAH due to trauma


©Amirsys, Inc

SAH due to reversible cerebral vasoconstriction syndrome (RCVS) Reversible, multifocal cerebral vasoconstrictions Clinical thunderclap headache +/- neurodeficits 20% shown on CT as small cortical SAH +/- IPH

CTA may show vasculitic pattern


Mimics of SAH

Pseudo-SAH from diffuse cerebral hypodensity

Intrathecal contrast medium Pus

Pseudo-SAH from severe brain edema ©Neurology 2012; 78:e54.


BRAIN

Shifting Gray-white differentiation

Symmetry

Hyper- or hypodensity


Brain Herniations: ��Midline Shift & Subfalcine

Displacement of brain beneath free edge of falx

Midline shift of septum pellucidum

Widening of contralateral CSF space at anterior falx


Brain Herniations: ��Transtentorial

Uncus moves downward across tentorium compressing brainstem

Unilateral or bilateral Obliteration of suprasellar

cistern

Effaced perimesencephalic cistern

Displaced midbrain


Brain Herniations: ��Tonsillar

Effacement of CSF cisterns around medulla

Inferior descent of cerebellar tonsils below foramen magnum


Gray-white Differentiation

Normal

Hypoxic-ischemic encephalopathy

* *

Different CT density because of water and lipid contents: GM more water and less lipid (“whiter” than WM)

Improved visibility with “narrow window” setting (images *)


ASPECTS��(Alberta Stroke Program Early CT Score) Assessing early ischemic changes in MCA territory

10 regions assigned a binary score of 0 or 1 depending on presence/absence of hypodensity

Normal CT’s ASPECTS = 10 points

www.AspectInStroke.com Ganglionic level Supraganglionic level


ASPECTS��(Alberta Stroke Program Early CT Score) ASPECTS of 7 or less – substantially increased risk of

thrombolysis-related parenchymal hemorrhage Poorer outcomes

Less likely to benefit from IV tPA Score >8 good candidates for IA, <5 typically not

M4

M5

M1

I

M2


Vasogenic edema 2/2 metastatic osteosarcoma

Increased GW Differentiation

White matter infarcts 2/2 CADASIL Images from JJ Downer et al. Clin Radiol 2009; 64:298

CADASIL = cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. “Subcortical infarcts

with diffuse WM ischemica in anterior temporal pole and external capsule in YOUNG individuals”


Brain Symmetry

Normal

Bilateral lesions Midline lesion Absence of a normal midline feature

Bilateral absence of normal features


Bilateral isodense SDHs Can be seen 2-6 weeks after onset or immediately in anemic patient


Symmetric pathology: Acute hypertensive encephalopathy (Posterior reversible encephalopathy syndrome)


Midline pathology: Sagittal sinus thrombosis


VENTRICLES

Hydrocephalus (first evident in dilation of temporal horns) Compression/shift of ventricular system


Hydrocephalus

Recognition of ventricular enlargement

Distinguish it from parenchymal atrophy “In hydrocephalus, sulci are effaced relative to ventricular size” Periventricular white matter low attenuation

Transependymal CSF spread due to increased ICP Level of obstruction


Hydrocephalus associated with SAH May be obstructive or nonobstructive.

Common and can occur early due to plugging of cerebral aqueduct and/or arachnoid granulations

Earliest sign = dilatation of temporal horns

* *

* *


Metastatic lung cancer S/P WBRT with brain atrophy and

progressive hydrocephalus

5 months after RT

* * * *


Raised ICP

Complete effacement of third ventricle

Severe diffuse brain swelling of any cause “Third ventricle should be visible in all age groups” Look for other signs: effacement of extra-axial CSF

spaces and tonsillar herniation


Intracranial hypotension due to CSF overshunting

Subdural collection, tonsillar herniation, dural venous sinus distension “venous distension sign”, sagging brainstem,

drooping splenium


SOME PEARLS & PITFALLS


Venous infarcts due to superior sagittal sinus thrombosis

Bilateral parasagittal lesions – do not forget venous sinus thrombosis


Hemorrhagic venous infarct due to superior sagittal sinus thrombosis

Cortical SAH – do not forget venous sinus thrombosis


Ruptured PCoA aneurysm presenting with IVH

Recognize early hydrocephalus

There should be nothing in the 3rd ventricle except clear black CSF


Ruptured AVM presenting with neck pain

Do not forget to look at posterior fossa in neck CT

Brain CT performed later confirming IVH

For educational purposes only 1 day 2 days 3 days

IA thrombectomy performed

CTA: phase 1 phase 2 phase 3

Left hemispheric symptoms for 1 hour

ASPECTS score = 9

IA Rx not recommended

mCTA: Right distal M1 occlusion Delayed collaterals 2 phases and decreased prominence/extent Collaterals score = 2 (intermediate)

Multiphase CTA is a promising tool to help making decision about IA Rx


Multiphase CTA in Stroke

Good leptomeningeal/pial collaterals beneficial in stroke

Repeated acquisitions after routine CTA = multiphase “Multiphase CTA”

Degree and extent of pial arterial filling of whole brain in a time-resolved manner

Assess collaterals better than one phase Avoid pitfalls of false occlusion on CTA


Multiphase CTA

147 patients

Interrater reliability n=30, k=0.81, P<.001

Menon BK, et al. Radiology 2015;275: 510


Multiphase CTA - Interpretation

Score Delayed Filling

Prominence Extent

Good 5 No Normal or increased Symmetric

4 1 phase Normal Symmetric

Intermediate 3 2 phases Normal Normal

1 phase Decreased Decreased

2 2 phases Decreased Decreased

1 phase No vessels in some areas

No vessels in some areas

Poor 1 3 phases A few vessels visible A few vessels visible

0 3 phases No vessels visible No vessels visible


For MCA territory occlusion Comparing with contralateral asymptomatic side


Multiphase CTA

Predicting clinical outcome at 24 hours

Best = baseline infarct volume (<80 vs. >80 mL) 2nd best = multiphase CTA (score >3 vs. <3)

Predicting clinical outcome at 90 days

Best = multiphase CTA (score >3 vs. <3) 2nd best = single-phase CTA (score >2 vs. <2)

Better than CTP mismatch ratio


For educational purposes only Images from Menon BK, et al. Radiology 2015;275: 510

78yo F, NIHSS 18, Rt hemispheric symptoms 1.5 hrs ASPECTS score = 8

mCTA: Rt M1 occlusion Delayed collaterals 1 phase Collaterals score = 4 (Good) IA Rx recommended

CTP: Blue = infarct core = 113 mL IA Rx not recommended

Incongruent mCTA and CTP IA Rx performed with success


Few Words on CT Perfusion

Acute stroke imaging

IV tPA: exclude hemorrhage IA tPA: confirm large-vessel occlusion, define/size “infarct core” (and grade collaterals)

Perfusion imaging does not measure “core”, it’s just probablistic – limited reliability for individual patient

No defined thresholds (different among vendors) New trials IA tPA successful because of new devices

and advanced imaging (occlusion, estimate core)


Summary (1)

No “safe” dose of radiation – it’s our responsibility

Concern, but not too much, of contrast-induced nephropathy (CIN)

Systematic CT interpretation “Blood Can Be Very Bad” Keep in mind: IPH due to venous sinus thrombosis Suspected SAH: CT & LP


Summary (2)

Use stroke window to identify subtle changes

Be aware of symmetric pathology: midline, bilateral symmetric

Be able to identify “mild” hydrocephalus New technique on the horizon- multiphase CTA for

acute stroke evaluation


“Training a neurologist today requires a careful balance between teaching traditional methods of observation-based diagnostic skills and the interpretation of newer and readily accessible imaging techniques.

Ong CJ. Ann Neurol 2015 Apr

In an environment in which head CT is often ordered before patients are even examined, it is difficult to imagine training a neurologist without its ubiquitous presence.”


“The challenge of this generation of neurologists is to maintain the framework of localization and disease categorization while optimizing the use of the technology at our disposal.

Addressing this issue may require a more deliberate structuring of resident education.”



“As a neurology trainee myself, I find the advice of the old guard to the new may embodied by the advice of my father, also a neurologist who trained in the 1970s.

‘You correlate the patient with the imaging,’ he would say, ‘not the imaging to the patient’ –”



THANK YOU VERY MUCH FOR YOUR ATTENTION!

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Neuro-imaging in Emergency Conditions