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7/25/2019 c.tscan Pathology by Faisal

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Basic interpretation of

CT-SCAN HEAD

DR. FAISAL NAWAZPGR MEDICAL UNIT-I

BY,


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MULTI SLICE HELICALCT SCANNER


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6ESSENTIAL C.T SCAN IMAGES TO

REMEMBER:


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6ESSENTIAL C.T SCAN IMAGES TO

REMEMBER:


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MR. X


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MR. STAR


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MR.SMILEY


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MR. SAD


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THE WORMS


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COFFEE BEAN


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VASCULAR TERRITORIES

The anterior ,middle and posterior cerebral arteries grossly supply the anterior,

middle and posterior parts of the brain from Mr. X to Mr. SAD. But from The

WOMS to The !O""## B#A$ le%el anterior cerebral artery supplies most of

the midline.


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PATHOLOGY PICKING


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HOW TO READ THE

CT-HEAD

&Ade'uacy of film

&(arenchyma&)entricle&!isterns&!ranial bones


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SYSTEMATIC APPROACH

*n medical school, +e are taught a systematic

techni'ue to interpret #!s -rate, rhythm, ais,

etc./ so that all aspects are re%ie+ed, and no

findings are missed.


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Th !"#"# $% #h!& &&&!$" !& #$ !"#'$()* +

&!!+' &+#!* #h$( $% *'+"!+ CT

!"#'/'#+#!$", 0+&( $" #h "$"!*1

BLOOD CAN BE VERY BAD

&B0OOD&!*ST#$S

&BA*$&)#$T*!0#S&BO$#


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BRAIN PARENCHYMA

!ompare the parenchyma of one side to the other.1Tilting of head +ill effect the symmetry.

0oo2 at the grey matter, +hite matter, at grey +hite3unction and the peri4%entricular region.

eference density is that of brain substance and !S".&5ypodense lesion could ha%e density less than brainand !S".

&5yperdensity greater than bone.&*sodensity comparable +ith brain.&5eterogenous -mied density/.


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HYPODENSITY ON CT SCAN

Higher than CSF but lower than brain tissue:&Evolution infarct.&Tumor.

&Abscess .&Resolving hematoma

Iso-ensit! to CSF:

&Chronic hematoma.&Chronic infarct.&Congenital c!st.


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HYPER-DENSITY ON

CT SCAN

Iso- or higher than bone:

&"ssification.

&Calcification.etallic.&Iatrogenic.&$loo %ooling.

&ess than bone but higher than brain tissue:&Hemorrhage.&Com%acte cellularit!.


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HEMORRHAGE


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6st'uestion7 *s blood present8

9nd'uestion7 *f so, +here is it8

:rd

'uestion7 +hat effect is itha%ing8


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Acute blood is bright +hite onAcute blood is bright +hite on!T -once it clots/.!T -once it clots/.

B$$( 0*$& !&$-("& +#

+//'$2!+# 3 45

Blood becomes hypo4dense

at approimately ; +ee2s.
http://www.nemcrad.org/InterestingCases/Neuro/case01/sub2.JPG


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COMMON SITES OF HYPERTENSIVE

BLEED ON C.T SCAN HEAD

6.BASA0 A$0*A

9.!##B#00


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HEMORRHAGE IN BASAL

GANGLIA


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HEMORRHAGE IN BASAL GANGLIA


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HEMORRHAGE IN CEREBELLUM


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HEMORRHAGE IN THE

THALAMIC REGION


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PONTINE HEMORRHAGE


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SUBARACHNOID HEMORRHAGE

Blood in the cisterns=cortical gyral

surface&Aneurysms responsible for >?4

@ of SA5&A)MCs responsible for ;4?&)asculitis accounts for small

proportion -6/&$o cause is found in 646?&9 +ill ha%e associated acute

hydrocephalus


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SUB-ARACHNOID HEMORRHAGE


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E/!()'+ H+#$+

&0ens shaped.

&Does not cross

sutures.

&!lassically described

+ith in3ury to middle

meningeal artery.

&0o+ mortality if treated

prior to

unconsciousness

- 9/.


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Acute right etra4dural

hemorrhage

-arro+heads/.

ight etradural hemorrhage.The collection is hyperdense

and isodense indicating both acute and

subacute hemorrhage. *n addition,

there is e%idence of subarachnoid

haemorrhage.


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&!rescent shaped.

&!rosses sutures, butdoes not cross midline.

&Acute subdural is amar2er for se%ere headin3ury. -Mortalityapproaches @/

&!hronic subduralusually slo+ %enousbleed and +elltolerated.

S)0()'+ H+#$+


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0arge acute right subdural

hematoma

-arro+heads/.

Shallo+ acute left subdural

hematoma -arro+s/.


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INFARCTION


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SEVEN STAGES:

&Acute-#ntirely normal/&0oss and blurring of gray +hite interface seen in

basal ganglion=thalamus= internal capsule.

-)anishing Basal ganglia sign/.

&0oss of insular ribbon in the temporal lobe.-*nsular ribbon sign/.&5yper4dense -M!A Dot sign/.&0ocaliEed mass effect, effacement of Sulci and

asymmetry of lateral %entricles.

&As edema progresses generaliEed mass effect.&5ypo4density.


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The !"&)+' '!00$" &!"refers to a

loss of grey +hite differentiation in

the lateral margin of the insular

corte -Finsular ribbonF/ and is

considered an early !T sign of M!A

infarction.

The insular corte is more

susceptible to ischaemia follo+ing

M!A occlusion than other portions of

the M!A territory because it has theleast potential for collateral supply

from the anterior cerebral and

posterior cerebral arteries.

INSULAR RIBBON

SIGN

RIGHT SIDE INSULAR RIBBON

SIGN AND VANISHING

BASALGANGLIA SIGN


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MCA DOT SIGN HYPERDENSE MCA SIGN


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TYPES

&*schemic.

&5emorrhagic.&5emodynamic.&0acunar.

FOGGING EFFECT:

*n roughly G of the cases,the infarct

may change from hypo4dense to

iso4dense. This has been termed

the Ffogging effectF on !T and isusually seen 94: +ee2s post ictus

during the sub4acute phase of

infarction and should resol%e on

subse'uent imaging. *) contrast

may ma2e the infarct more

conspicuous.


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THALMIC INFARCTION


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INFARCTION IN LEFT MIDDLE

CEREBRAL ARTERY


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BASAL GANGLIA INFARCTION


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CEREBRAL VENOUS SINUS

THROMBOSIS

&!lassically presents +ith sudden, se%ere headache,

+orsened by coughing and associated +ith %omiting.&"ocal neurological deficit may be seen if %enous infarction

occurs.

&!ranial ner%e palsies are characteristic.&SeiEures may occur.&Sigmoid sinus thrombosis causes cerebellar signs and

lo+er cranial ner%e palsies.&(eriorbital oedema and chemosis are seen +ith ca%ernous

sinus thrombosis.&"undoscopy may sho+ papilloedema or retinal %ein

thrombosis.


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Sagittal sinus thrombosis7 Scans pre4 and post4contrast.

On the pre4contrast study , hyper4dense material is seen +ithin the sagittal sinus.This is an unreliable sign for acute thrombus. 5o+e%er, follo+ing contrast, the

HdeltaC sign is clearly %isible.


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)enous hemorrhage in

the left

"ronto4parietal corte

)enous lesions aredifferentiated from arterial by

these facts7&They are usually present in

the superficial slides.&These lesions occur in an

area +hich is not

characteristic of any arterial

territory.

&They donCt ha%e any definiteshape.


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EDEMA


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&rey4+hite matter differentiationis maintained and the edema

in%ol%es mainly +hite matter,

etending in finger4li2e fashion.

&*t is most fre'uently seen

around Brain Tumors -both

primary and secondary/ and

!erebral Abscesses.

&*n this type of edema, the

blood brain barrier is

disrupted.

VASOGENIC EDEMA


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CYTOTOXIC EDEMA

&*n this type of edema, the

blood brain barrier is intact.

&*t is due to a cellular s+elling

from lac2 of AT(, that istypically seen in area

of cerebral ischemia

or cerebral hypoia.

&0oss of grey +hite matter

differentiation -as it mainly

affects grey matter/ I

effacement of sulcal space.


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RING ENHACNING LESIONS


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6.!erebral abscess.

9.Tuberculoma.

:.Metastasis.

;.Tooplasmosis

?.!.$.S lymphoma -in immuno4compromised patient/.

J.lioblastoma multiforme.

>.!ystic astrocytoma.@.$euro4cysticercosis

K.Sub4acute infarct = hemorrhage = contusion.

6.Demyelination -incomplete ring/.

66.adiation necrosis.

69.(ost4operati%e change.

Mneumonics for this are TRAGIC M.D =MAGIC D.R

DIFFERENTIALS


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#nhancing +all characteristics7&Thic2 and nodular +ith rough inner margin fa%ors neoplasm.&Thin and regular +ith smooth inner margin fa%ors abscess.&*ncomplete ring often opened to+ard the corte fa%ors

demyelination.

Surrounding oedema7tensi%e oedema relati%e to lesion siEe fa%ors abscess.&*ncreased perfusion fa%ors neoplasm -metastases or primary

cerebral malignancy/.

$umber of lesions7&Similar siEed rounded lesions at grey +hite matter 3unction fa%ors

metastases or abscesses.&Small -649cm/ lesions +ith thin +alls especially if other calcific

foci are present suggest neuro4cysticercosis.

DIFFERENTIATING FEATURES


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A L Metastasis

B L Abscess! L adiation necrosisD L BM# L Demyelination" L !ontusion


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GLIOBLASTOMA MUTLIFORME

*rregular thic2 margins ha%ing an irregular hypo4dense centre -representing

necrosis/ +ith mar2ed mass effect and surrounding %asogenic oedema.


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VENTRICLES

*nspect the %entricles for7&SiEe.

&Shape.&Spatial relationship.&The presence of the blood.


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C.S.F PRODUCTION

&(roduction occurs in the

choroid pleus of the lateral

%entricles"oramen of

Monro***rd )entricle

Ac'ueduct of Syl%ius*)th)entricle"oramen of

0ush2a = MagendiSub4

Arachnoid space.

&Adult !S" %olume is appro.

6? ccCs.&Adult !S" production is

appro. ?4> ccCs per day.


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5ydrocephalusresults from an ecess of !S", due to an imbalance

bet+een !S" production and absorption, resulting in increased intra4

%entricular pressure.

!ommunicating hydrocephalus is caused by ele%ated intra4

%entricular pressure secondary to obstruction of !S" flo+ beyond the

outlet of ;th %entricle.

This may be due to impeded !S" flo+ o%er the cerebral con%eities

and=or impeded re4absorption of !S" by the Arachnoid )illi.

$on4communicating hydrocephalus is caused by bloc2age of !S"flo+ +ithin the %entricular system, +ith dilatation proimal to the

obstruction.

Often referred to as obstructi%e hydrocephalus.

HYDROCEPHALUS


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COMMUNICATING

HYDROCEPHALUS


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NON-COMMUNICATING HYDROCEPHALUS


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0ateral %entricles ha%e three horns each the frontal, occipital, andtemporal horns.

The frontal and occipital horns are easily identified, but thetemporal horns can be a little bit tric2y. They are not al+ays %isible.

5o+e%er, symmetry is the 2ey. *f you see one, you should see theother. They +ill be located slightly anterior to the petrous ridge, on

approimately the same slice, and are shaped li2e an H0C.

&Obliteration of these is caused by7Medial mo%ement of the temporal lobes -secondary to mass effector hematoma/ tumor, or prior surgery.

&*ncrease in the siEe of the temporal horns is due to7Atrophy or *ncreased !S" - i.e. 5ydrocephalus/.


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BONE

&0oo2 at the scout film as it is a free lateral s2ullplain radiograph.

&The bone +indo+s should be eamined fore%idence of fracture as a clue to underlyingintracranial pathology. Be sure to inspect the softtissues for s+elling and defects -i.e. lacerations/.

&Determine if there are any depressed fractures,or pieces of bone missing -i.e. pre%ious surgery/.


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0eft parietal bone fracture

-arro+heads/ +ith mar2ed

o%erlying

soft tissue contusion.

Depressed s2ull

fracture


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!omple %ault fracture Bilateral temporal bone

fractures


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CISTERNS

!isterns are !S" collections, 3ac2eting the brain.

"our 2ey cisterns must be eamined for blood,asymmetry and effacement -as +ith increased *!(.

These are76.!ircum4mesencephalic = Ambient7 ring around themidbrain.9.Supra4sellar7 Star shaped at circle of +illis:.Syl%ian cistern7 bet+een temporal and frontal lobe.;.Nuadrigeminal7 W shaped ay the top of midbrain


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&I% "$ 0$$(!& &",&A *!'"&+' /'&"# +"( $/",

&Th 0'+!"!& '!* 4!#h "$'+'+-4h!# (!%%'"#!+#!$",&Th 7"#'!*&+' '!*

4!#h$)# (!+#!$",&A"( #h' !& "$ 0$"%'+*#)',

&Th" #h' !& "$ '"#(!+"$&!& %'$ #h CT &*+".

BLOOD CAN BE VERY BAD


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SELF ASSESSMENT

CASE 3


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!ase 6.A shallo+ hyper4dense collection is seen o%er the right frontal

lobe-arro+heads/.

Diagnosis7Acute subdural hemorrhage.

CASE 3


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CASE 8

!ase 9. 0arge area of lo+ density, in%ol%ing both grey and +hite matter, +ithin

the left middle cerebral artery territory -arro+heads/.

Diagnosis7Acute left middle cerebral artery territory infarct.

CASE 9


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CASE 9

!ase :. "ocal area of hyper4density centered upon the right thalamus and

lentiform nucleus -arro+head/.

Diagnosis7Acute parenchymal hemorrhage. This type of hemorrhage

has a strong association +ith uncontrolled hypertension.

CASE


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CASE

!ase ;.A shallo+ hyper4dense collection is seen o%er the left cerebral

conca%ity -arro+heads/.

Diagnosis7Acute subdural hemorrhage.

CASE ;


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CASE ;

!ase ?.Subtle linear hyperdensity is seen outlining se%eral sulci +ithin the

left cerebral hemisphere -arro+heads/.

Diagnosis7Acute subarachnoid haemorrhage.

CASE 6


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CASE 6

!ase J.Aial scan %ie+ed on Hbone +indo+sC, demonstrating sharply

marginated defects +ithin the left occipital bone -arro+heads/.

Diagnosis7 0eft occipital fracture.

CASE


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CASE . *nsular ribbon sign in the left insular corte and in the immediately

ad3acent cortical and sub4cortical portions of the left temporal region.

Diagnosis7Acute *nfarction


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CASE =

!ase @.

6. 5yper4dense bicon%e collection o%er the

right temporal lobe -straight

+hite arro+heads/.

9. 0inear hyper4density outlining the basal

cisterns -cur%ed arro+heads/.:. "ocal parenchymal hyperdensity -blac2

arro+heads/.

Diagnosis7Acute etra4dural hemorrhage

+ith additional subarachnoid

hemorrhage and parenchymal contusions.

CASE >


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!ase K.0arge area of lo+ density, in%ol%ing both grey and +hite matter,

+ithin the left cerebellar hemisphere -arro+heads/. Associated compression

of the fourth %entricle due to mass effect.

Diagnosis7Acute left cerebellar infarct.

CASE 3?


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CASE 3?

!ase 6. 5yper4dense focus +ithin the fourth %entricle -arro+/.

Diagnosis7Acute intra4%entricular hemorrhage.

CASE 33


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CASE 33

!ase 66. This plain !T scan of the head sho+s a cerebellar %ermian mass

+ith associated %asogenic edema and moderate cerebral atrophy.

M..* done sho+s a ring enhancing lesion.

Differentials7 88888888

CASE 38


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CASE 38

!ase 69. This !T scan of the head sho+s mied density lesion composed

of coarse calcification, and faintly hyper4dense %essels -arro+head/. Mar2ed

enhancement post4contrast.

Differentials7Arterio4%enous malformation.


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!ase 6:7 Mied density crescent shaped area o%er the right cerebral

conca%ity +ith peri4focal edema and prominent sulci gyri on left side.

Diagnosis7 ight sided Acute on chronic Sub4dural hematoma.

CASE 39


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