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GAMBARAN CT SCAN

Stroke Iskemik dan Gambaran Ct Scan


Stroke merupakan penyebab utama kematian di seluruh dunia. Pada kasus stroke iskemik hiperakut
(0-6 jam), CT scan biasanya tidak sensitif dalam mengidentifi kasi infark serebri; namun, cukup sensitif
dalam mengidentifi kasi berbagai bentuk perdarahan intrakranial akut dan lesi makroskopik lain yang
menjadi kontraindikasi penggunaan terapi trombolitik. Gambaran infark hiperakut pada CT scan berupa
pendangkalan sulkus disertai menghilangnya batas substansia alba dan grisea pada infark kortikal
superfi sial (mis., tanda insular ribbon), hipodensitas ganglia basalia (mis., hipodensitas nuklei
lentiformes), tanda hiperdensitas arteri serebri media (middle cerebral artery, MCA), dan tanda Sylvian
dot. Dalam periode akut (6-24 jam), perubahan gambaran CT scan non-kontras akibat iskemia menjadi
makin jelas. Distribusi pembuluh darah yang mengalami infark juga makin jelas pada fase ini. Pada
periode subakut (1-7 hari), terjadi perluasan edema dan efek massa yang menyebabkan pergeseran
jaringan infark ke lateral dan vertikal (pada kasus infark yang mengenai daerah pembuluh darah besar).
Infark kronis ditandai dengan hipodensitas yang mencolok dan berkurangnya efek massa pada
gambaran CT scan; densitas daerah infark sama dengan cairan serebrospinal.

Kata kunci: stroke iskemik, infark hiperakut, infark akut, infark subakut, infark kronis

PENDAHULUAN
Survei Departemen Kesehatan RI pada 987.205 subjek dari 258.366 rumah tangga di 33 provinsi
menunjukkan bahwa stroke merupakan penyebab kematian utama pada usia di atas 45 tahun (15,4%
dari seluruh kematian).
Penelitian prospektif tahun 1996/1997 mendapatkan 2.065 pasien stroke di 28 rumah sakit di Indonesia.
Di Yogyakarta, dari 1.053 kasus stroke di 5 rumah sakit, tercatat angka kematian sebesar 28,3%.
Mortalitas pasien stroke di RSUP Dr. Sardjito Yogyakarta menduduki peringkat ketiga setelah penyakit
jantung koroner dan kanker.
Pada tahun 1995, National Institute of Neurologic Disorders and Stroke (NINDS) melaporkan
penggunaan aktivator plasminogen jaringan rekombinan (recombinant tissue plasminogen activator, rt-
PA) dalam 3 jam sejak onset gejala dapat memperbaiki hasil akhir terapi. Hal ini menyebabkan
pentingnya dilakukan CT scan dini untuk menyingkirkan adanya perdarahan intrakranial dan penyebab
non vaskular, misalnya tumor serebri (karena t-PA meningkatkan risiko perdarahan intrakranial).1-3

DEFINISI
Stroke adalah gangguan fungsional otak fokal maupun global akut, lebih dari 24 jam, berasal dari
gangguan aliran darah otak dan bukan disebabkan oleh gangguan peredaran darah otak sepintas,
tumor otak, dan stroke sekunder karena trauma maupun infeksi.
Stroke dengan defi sit neurologik yang terjadi tiba-tiba dapat disebabkan oleh iskemia atau perdarahan
otak. Stroke iskemik disebabkan oleh oklusi fokal pembuluh darah otak yang menyebabkan
berkurangnya suplai oksigen dan glukosa ke bagian otak tertentu. Oklusi dapat berupa trombus,
embolus, atau tromboembolus, menyebabkan hipoksia sampai anoksia salah satu daerah pendarahan
otak tersebut. Stroke hemoragik dapat berupa perdarahan intraserebral atau perdarahan
subarakhnoid.4,5

PERUBAHAN GAMBARAN CT SCAN PADA STROKE ISKEMIK


Infark Hiperakut
Pada kasus stroke iskemik hiperakut (0-6 jam setelah onset), CT scan biasanya tidak sensitif
mengidentifi kasi infark serebri karena terlihat normal pada >50% pasien; tetapi cukup sensitif untuk
mengidentifi kasi perdarahan intrakranial akut dan/atau lesi lain yang merupakan kriteria eksklusi terapi
trombolitik.
Gambaran CT scan yang khas untuk iskemia serebri hiperakut adalah sebagai berikut2,3,5-7:
Gambaran pendangkalan sulcus serebri
(sulcal eff acement)
Gambaran ini tampak akibat adanya edema difus di hemisfer serebri. Infark serebral akut menyebabkan
hipoperfusi dan edema sitotoksik. Berkurangnya kadar oksigen dan glukosa seluler dengan cepat
menyebabkan kegagalan pompa natrium-kalium, yang menyebabkan berpindahnya cairan dari
ekstraseluler ke intraseluler dan edema sitotoksik yang lebih lanjut. Edema serebri dapat dideteksi
dalam 1-2 jam setelah gejala muncul. Pada CT scan terdeteksi sebagai pembengkakan girus dan
pendangkalan
sulcus serebri.5,7

Menghilangnya batas substansia alba dan substansia grisea serebri Substansia grisea merupakan
area yang lebih mudah mengalami iskemia dibandingkan substansia alba, karena metabolismenya
lebih aktif. Karena itu, menghilangnya diferensiasi substansia alba dan substansia grisea merupakan
gambaran CT scan yang paling awal didapatkan. Gambaran ini disebabkan oleh influks edema pada
substansia grisea. Gambaran ini bisa didapatkan dalam 6 jam setelah gejala muncul pada 82% pasien
dengan iskemia area arteri serebri media.3,7,8
Tanda insular ribbon
Gambaran hipodensitas insula serebri cepat tampak pada oklusi arteri serebri media karena posisinya
pada daerah perbatasan yang jauh dari suplai kolateral arteri serebri anterior maupun posterior.3
Hipodensitas nukleus lentiformis
Hipodensitas nukleus lentiformis akibat edema sitotoksik dapat terlihat dalam 2 jam setelah onset.
Nukleus lentiformis cenderung mudah mengalami kerusakan ireversibel yang cepat pada oklusi bagian
proksimal arteri serebri media karena cabang lentikulostriata arteri serebri media yang
memvaskularisasi
nukleus lentiformis merupakan end vessel.3

Tanda hiperdensitas arteri serebri media


Gambaran ekstraparenkimal dapat ditemukan paling cepat 90 menit setelah gejala timbul, yaitu
gambaran hiperdensitas pada pembuluh darah besar, yang biasanya terlihat pada cabang proksimal
(segmen M1) arteri serebri media, walaupun sebenarnya bisa didapatkan pada semua arteri. Arteri
serebri media merupakan pembuluh darah yang paling banyak mensuplai darah ke otak. Karena itu,
oklusi arteri serebri media merupakan penyebab terbanyak stroke yang berat. Peningkatan densitas ini
diduga akibat melambatnya aliran pembuluh darah lokal karena adanya trombus intravaskular atau
menggambarkan secara langsung trombus yang menyumbat itu sendiri. Gambaran ini disebut sebagai
tanda hiperdensitas arteri serebri media (Gambar 4).1-3,5,6

Tanda Sylvian dot menggambarkan adanya oklusi distal arteri serebri media (cabang M2 atau M3)
yang tampak sebagai titik hiperdens pada fi sura Sylvii (Gambar 5).5,7
Infark Akut
Pada periode akut (6-24 jam), perubahan gambaran CT scan non-kontras akibat iskemia makin jelas.
Hilangnya batas substansia alba dan substansia grisea serebri, pendangkalan sulkus serebri,
hipodensitas ganglia basalis, dan hipodensitas insula serebri makin jelas.
Distribusi pembuluh darah yang tersumbat makin jelas pada fase ini.1

Infark Subakut dan Kronis


Selama periode subakut (1-7 hari), edema meluas dan didapatkan efek massa yang menyebabkan
pergeseran jaringan infark ke lateral dan vertikal. Hal ini terjadi pada infark yang melibatkan pembuluh
darah besar.
Edema dan efek massa memuncak pada hari ke-1 sampai ke-2, kemudian berkurang. Infark kronis
ditandai dengan gambaran hipodensitas dan berkurangnya efek massa. Densitas daerah infark sama
dengan cairan serebrospinal (Gambar 6).

RINGKASAN
Pada pasien dengan gejala klinis stroke, pemeriksaan CT scan perlu dilakukan untuk menyingkirkan
perdarahan intrakranial dan penyebab nonvaskular lain, karena terapi aktivator plasminogen jaringan
rekombinan untuk stroke iskemik dapat meningkatkan risiko perdarahan intrakranial.

Pada kasus stroke iskemik hiperakut (0-6 jam setelah onset), CT scan terlihat normal pada >50%
pasien. Gambaran CT scan yang khas untuk iskemia serebri antara lain pendangkalan sulkus serebri,
menghilangnya batas substansia alba dan substansia grisea, misalnya tanda insular ribbon;
hipodensitas
nukleus lentiformis, hiperdensitas arteri serebri media, dan tanda Sylvian dot. Pada infark akut (6-24
jam), gambaran-gambaran tersebut dapat terlihat makin jelas. Selama periode subakut (1-7 hari),
edema meluas dan didapatkan efek massa yang menyebabkan pergeseran jaringan yang mengalami
infark ke lateral dan vertikal. Infark kronis ditandai dengan gambaran hipodensitas dan berkurangnya
efek massa; densitas daerah infark sama dengan cairan serebrospinal.

DAFTAR PUSTAKA
1. Xavier AR, Qureshi AI, Kirmani JF, Yahia AM, Bakshi R. Neuroimaging of Stroke: A Review. South
Med J. 2003;96(4). http://www.medscape.com/viewarticle/452843
2. Choksi V, Quint DJ, Maly-Sundgren P, Hoeff ner E. Imaging of Acute Stroke. Applied Radiology.
2005;34 (2):10-19. Available at: http://www.medscape.com/viewarticle/500443_print
3. Tomandl BF, Klotz E Handschu R Stemper B, Reinhardt F, Huk WJ, Eberhardt KE, Fateh-Moghadam
S. Comprehensive Imaging of Ischemic Stroke with Multisection CT. RadioGraphics 2003;
23:565592. Available at: http://radiographics.rsna.com/content/23/3/565.full.pdf+html
4. Setyopranoto I. Stroke: Gejala dan Penatalaksanaan. CDK 2011; 38 (4).
5. Warren DJ, Musson R, Connoly DJA, Griffi ths PD, Hoggard N. Imaging in Acute Ischaemic Stroke:
Essential For Modern Stroke Care. Postgrad Med J. 2010;86:409-18. Available at: http://pmj.
bmj.com/content/86/1017/409.full.pdf
6. Hakimelahi R, Gonzales RG. Neuroimaging of Ischemic Stroke with CT and MRI: Advancing Towards
Physiology-Based Diagnosis and Therapy. Expert Rev Cardiovasc Ther. 2009;7(1):29-48.
Available at: http://www.medscape.com/viewarticle/587073
7. Harrigan MR, Deveikis JP. Trombolysis for Acute Ischemic Stroke. In: Handbook of Cerebrovascular
Disease and Neurointerventional Techniques. New York: Humana Press, 2009. p. 326-
30.
8. Foundation for Education and Research in Neurological Emergencies (FERNE). Neuroimaging in
Stroke. 2003. Available at: http://www.ferne.org/Lectures/neuroimaging%200501.htm
Posted by fajrucmedicine at 2:20 AM
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Labels: definisi stroke iskemik, ifark akut, storke iskemik, Stroke iskemik dan gambaran ct scan

2 comments:
Sir,

Intravenous immunoglobulin (IVIg) is used in the treatment of a variety of immune-mediated


disorders of the nervous system. The reported rate of serious adverse events with the use of IVIg
is less than 5% and stroke is a rare adverse event.[1]

A 62-year-old male presented with a complaint of legs weakness of one day duration. His
symptoms initially started as burning pain in his legs. Over the next 24 h, he developed leg
weakness which later spread to his trunk and upper limbs. He had been treated for viral bronchitis
ten days prior to this admission. The neurologic examination revealed a motor power of 3/5 in
lower limbs and 4/5 in upper limbs with diminished deep tendon reflexes in all the limbs. Cranial
nerves and sensory system were normal. Cerebrospinal fluid (CSF) analysis showed albumin-
cytologic dissociation with CSF protein of 54 and WBC of 9. Electrodiagnostic studies showed motor
and sensory polyneuropathy with mixed axonal and demyelinating features consistent with
diagnosis of GBS. Patient received IVIg 0.4 g/kg/day for 5 days. He had improvement in his
muscle strength and was discharged home in a stable condition.

Five days after completing the course of IVIg, patient presented again with bilateral blurring of
vision and bifrontal headache of four hours duration. His visual blurring was sudden in onset and
affected both the eyes simultaneously. By the time he presented to the emergency department,
his visual blurring had already resolved but he had persistent headache. Headache was bifrontal,
throbbing in nature, severe in intensity with no aggravating or relieving factor. He denied any
associated nausea or vomiting eye pain, haloes or floaters in the eyes. At the time of admission,
his blood pressure was 163/84 mmHg. Physical examination showed patient in mild distress.
Fundus examination showed no evidence of papilledema. Central and peripheral visual fields were
full to confrontation and visual equity was normal. Neurological examination was essentially
normal. Non-contrast enhanced computerized tomography (CT) scan of the brain showed acute
bilateral occipital infarcts[Figure 1]. A follow-up magnetic resonance imaging (MRI) of the brain
showed acute bilateral suboccipital hyperintense lesions [Figure 2]. Plasma viscosity was 1.87
centipoise (cp) (normal range 1.5-1.72). MR angiography of the cerebral blood vessels and
transesophageal echocardiography were normal. Since the patient was outside the three-hour
window for thrombolytics and his symptoms had already been resolved, he was managed
conservatively with antiplatelet therapy. After an extensive negative work up, patient's stroke was
attributed to IVIg therapy and he was discharged home in a stable condition.

Figure 1: CT head with arrows showing low-attenuation changes in the


parietal and occipital lobes suggestive of acute to subacute bilateral
occipital infarcts

Click here to view

Figure 2: MRI brain with arrows showing edema in the subcortical white
matter of both the right and left posterior temporal and occipital
regions, likely of an ischemic nature

Click here to view

Stroke is a very rare but serious complication of IVIg therapy. [1] In our patient, the association
between stroke and administration of IVIg is suggested by timing of stroke within five days of IVIg
administration, high plasma viscosity, and no other risk factors for stroke. In the series of 16
patients described by Caress et al., [1] the average age was 66.1 years, and 69% of them were
men. Fifteen of the 16 patients had one or more stroke risk factors that may predispose to stroke.
Of the 16 patients, 14 patients developed stroke with 24 h of IVIg infusion. The most commonly
proposed mechanism for IVIg-related stroke is an increase in serum viscosity leading to impaired
blood flow. [1] High concentration and rapid infusion rate of IVIg as well as osmolarity of the
solution are also thought to be the predisposing factors for thrombotic events. IVIg is also thought
to increase platelet count, activate platelets, and increase fibrinogen levels. Some preparations
may also increase concentration of factor XI.

Optimal treatment of stroke in this setting is unknown but patients have been treated with
antiplatelet agents and thrombolytic therapy. Successful use of tissue plasminogen activator has
been documented in cerebral and peripheral arterial thrombosis after treatment with IVIg. [2] The
association between IVIg use and thrombotic complications should be considered when treating
patients with IVIg, particularly in patients at risk for thrombosis. To decrease the risk of
thrombotic events in high-risk patients, slower rates of infusion and dosages less than 400 mg/kg
per day have been suggested. [3] Concomitant administration of blood products is usually not
recommended, and IVIg should be used with great caution in patients with known
gammopathies. [3]

References

1. Caress J, Cartwright M, Donofrio P, Peacock JJ. The clinical features of 16 cases of stroke
associated with administration of IVIg. Neurology 2003;60:1822-4.

2. Okuda D, Flaster M, Frey J, Sivakumar K. Arterial thrombosis induced by IVIg and its
treatment with tPA. Neurology 2003;60:1825-6.
[PUBMED] [FULLTEXT]
3. Go R, Call T. Deep venous thrombosis of the arm after intravenous immunoglobulin infusion:
case report and literature review of intravenous immunoglobulin-related thrombotic
complications. Mayo Clin Proc 2000;75:83-5.

TIME COURSE OF ISCHEMIC STROKE ON NON-


ENHANCED CT.
February 11, 2013 by Teddy Poh in Review, Uncategorized.

The subset of ischemic stroke can be divided into hyperacute, acute, subacute and chronicstroke based
on timing from the onset of stroke symptoms. It is generally a definition of time which is the first 6 hours,
6-48 hours, 48h to weeks, and weeks to months respectively [ref1]. However such duration does not have
general agreement among various articles [ref2][ref3][ref4][ref5]. Thus, the author recommends that
readers should not be obsessed with the specific duration of time as it does not carry a significant clinical
implication. This is because, the computer tomography (CT) scans finding on each stage varies among
individual. It depends on the size, duration and severity of infarct, the metabolic state of brain tissues and
the presence of collateral arteries.
The ischemic changes detected by unenhanced CT are caused by cytotoxic edema (occurred within 30
minutes) attributed to lactic acidosis and failure of cellular membranes ion pumps. This results in
redistribution of water from extracellular to intracellular space. This eventually reduces the Hounsfield
values (The degree of attenuation detected by CT is measured by Hounsfield scale in HU). For every 1%
increase in tissue water content, there is a reduction of X-ray attenuation by 3-5% which is equivalent to
a reduction of 2.5 HU on CT. Tissue water content is increased by 0.9% at 2.5 hour and 2% at 4 hour.
These small changes are difficult to be detected by human naked eyes. [ref6][ref7]

Hyperacute and Acute Stage


The CT findings of ischemic stroke depend on the artery and site involved. The CT findings during the first
3-6 hour (hyperacute) include loss of gray-white matter differentiation of cortical gyrus, basal ganglia
or insula; loss of cortical sulci or narrowing of the Sylvian fissure;compression of ventricular system
and basal cisterns; area of hypodensity; andhyperdensity in a circle of Willis
vessel [ref1][ref6][ref8][ref9][ref10][ref11]. However, within 3 hours of symptoms onset, these early
ischemic changes are found only in 31-53% of the patient but improves at 6 h with sensitivity of 67%
[ref6][ref12]. Although normal CT brain might be found, it does not excludes the presence of ischemic
stroke as it has a low negative predictive value (27%) in the first 6 hour [ref12]. If middle cerebral artery
(MCA) is involved, it has been stated that up to 75% of the cases will have abnormal CT findings within 3
hour [ref8]. However in cases of lacunar infarct, only approximately 50% shows abnormal CT findings
within 48 hour [ref 12][ref13][ref14].

Image above shows


the early CT sign (<6h) of ischemic stroke with loss of gray-white matter differentiation in basal ganglia
(left) and a diffuse cerebral swelling with los of cortical sulci and compression of ventricular system
(right). Image obtained from [ref2].
Image above shows the early CT sign (<6h) of ischemic stroke with hyperdensity of MCA representing an
acute embolus lodged into it (left) known as hyperdense MCA sign. Image on the right shows the
hypodensity of insular cortex known as insular ribbon sign. Image obtained from [ref2].

Image above is a CT of
ischemic stroke at 24h after onset, showing a hypodense area and enlargement of left temporal lobe
which compresses the left Sylvian fissure. Image obtained from [ref1].
Image above shows
the CT finding of left hyperdense MCA sign, and a dot sign (right) presence at the left Sylvian fissure.
Image obtained from [ref8].
Due to the fact the ischemic stroke is a dynamic process, the CT findings change over time. The early
ischemic changes can be present anytime up to 72hour regardless of the initial presence of CT findings
[ref1]. Hypodensity area detected by CT previously may gradually expand, involving both gray and white
matter of the brain.

Image above is the


contrast-enhanced CT image at 4h after stroke onset (left) and non-enhanced CT at 32h (right) of the
same patient. This demonstrate the expansion of hypodensity area as time progresses. Image obtained
from [ref11].
Subacute Stage
As time progresses, in the subacute phase, brain swelling and mass effect will gradually build up within a
week followed by gradual improvement beginning from that 1 week onward. These are not easily picked
up by human eyes on CT. Initial hypodensity detected by CT usually remains during this phase. However,
an interesting phenomena sometimes occurred during this phase known as CT fogging effect where
hypodensed infarcted area disappear, becoming isodense. This is probably dues to resolution of edema
in the infarcted area. This usually occurs between 2-6 weeks after the onset of stroke. Such disappeared
infarct will reappear in later phase in a form of tissue cavitation (encephalomalacia).
[ref1][ref2][ref3][ref6][ref16]
In addition to that, there is also a risk of hemorrhagic transformation in 15-20% of the cases during this
period of time. Most of the time, this occurred within 4-6 days after onset of stroke. Once happened, the
hyperdensity CT image may persist up to 8-10weeks. [ref1][ref6]

Image above shows


the CT result demonstrating the fogging effect occurs during subacute phase. Left CT image is obtained
at 36h with bilateral occipital hypodensities. Right image is taken at 18 days showing the isodense
appearance of previous infarct. Image obtained from [ref6].

Image above shows


the CT result demonstrating the hemorrhagic transformation with foci of hemorrhage at the right post
central gyrus (right). Image obtained from [ref7].
Chronic Stage
In chronic stage, which has vaguely defined period (weeks to months), the damaged necrotic tissue is
resorbed. This results in formation of encephalomalacia accompanied by gliosis of adjacent brain tissue.
Associated with this is dilation of ventricular system of affected part, though usually found in relatively
large infarct. These pathological finding could be picked up by non-enhanced CT and MRI.
[ref1][ref2][ref3]

Image above shows


the CT picture of various location of ischemic stroke at chronic phase, demonstrating the
encephalomalacia. Image obtained from [ref1].
This post is dedicated to my friend, Kenneth Tee.

References

1. Valery N. Kornienko and Igor N. Pronin, eds. Diagnostic Neuroradiology. First edition. Springer, Leipzig,
Germany. 2009.

2. Mara M. Kunst and Pamela W. Schaefer. Ischemic stroke. Radiol Clin N Am. 2011; 49:1-26. Doi:
10.1016/j.rcl.2010.07.010
3. D. Nagaraja and N. Karthik. Imaging in stroke. Medicine Update. 2011; 214-220.

4. K. Aho et al. Cerebrovascular disease in the community: results of a WHO collaborative study. Bull
WHO. 1980;58:113130

5. John R. Lynch et al. Novel Diagnostic Test for Acute Stroke. Stroke. 2004; 35: 57-63. Doi: 10.1161/
01.STR.0000105927.62344.4C

6. R.G Gonzalez et al. Acute ischemic stroke: imaging and intervention. Second edition. Springer, New
York, NY. 2011.

7. David Vu and Michael H. Lev. Noncontrast CT in acute stroke. Semin Ultrasound CT MRI. 2005; 26:380-
386.
8. Keith W. Muir et al. Imaging of acute stroke. Lancet Neurology. 2006; 5:755-768.

9. Joanna M. Wardlaw and Orell Mielke. Early signs of brain infarction at CT: observer reliability and
outcome after thrombolytic treatment, systematic review. Radiology. 2005; 235:444-453

10. Gyanendra Kumar et al. Penumbra, the basis of neuroimaging in acute stroke treatment: current
evidence. Journal of Neurological Sciences. 2010; 288:13-24.

11. James M. Provenzale et al. Assessment of the patient with hyperacute stroke: imaging and therapy.
Radiology. 2003; 229:347-359.

12. Jose G. Merino and Steven Warach. Imaging of acute stroke. Nature Review Neurology. 2009; 6:560-
571

13. C. Stapf et al. Predictive value of clinical lacunar syndromes for lacunar infarcts on magnetic
resonance brain imaging. Acta Neurologica Scandinavica. 2000; 101(1): 12-18

14. B. Norrving and S. Cronqvist. Clinical and radiologic features of lacunar versus nonlacunar minor
stroke. Stroke. 1989; 20:59-64

15. Kavian Ghandehari and Zahra Izadi. Clinical evaluation of 625 lacunar syndrome patients. Turk J Med
Sci. 2009; 39(4):607-612.

16. H. R. Jager. Diagnosis of stroke with advanced CT and MR imaging. British medical bulletin. 2000;
56(2):318-333
CT

Axial non-contrast

Hypodensity in the left cerebellar hemisphere, in the territory of the left PICA.
48 hours later
Modality: CT