KATA PENGANTAR

Assalamu’alaikum Wr.Wb
Puji syukur kehadirat Allah SWT, atas rahmat-Nya sehingga penulis bisa
menyelesaikan penyusunan Karya Tulis Ilmiah yang berjudul “FATTY LIVER”. Penulisan
karya ilmiah ini merupakan salah satu tugas yang diberikan dalam mata kuliah Skill’s Lab
Modul Gawat Darurat Medik di Universitas Baiturrahmah.
Dalam Penulisan karya ilmiah ini penulis merasa masih banyak kekurangan baik pada
teknis penulisan maupun materi, mengingat akan kemampuan yang penulis miliki. Untuk
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ilmiah ini, khususnya kepada dosen pembimbing yang telah memberikan tugas dan petunjuk
kepada penulis, sehingga penulis dapat menyelesaikan tugas ini.
Penulis sangat berharap agar karya ilmiah ini dapat dijadikan acuan bagi dosen
pembimbing, dan mahasiswa FK UNBRAH agar dapat menyelenggarakan pendidikan
dokter yang berkualitas seperti yang kita harapkan bersama. Semoga karya tulis ilmiah ini
bermanfaat bagi kita semua.
Wassalamu’alaikum Wr.Wb

Padang, Januari 2016

Penulis
ABSTRACT

Stroke is a leading cause of death worldwide. In the case of hyperacute ischemic

stroke (0-6 hours), CT scan is usually not sensitive in identifying cerebral infarction;
however, quite sensitive in identifying various forms of acute intracranial hemorrhage and
other macroscopic lesions contraindicate the use of thrombolytic therapy. Picture infarction
hyperacute on CT scan in the form of silting sulcus accompanied by the disappearance of
boundaries white matter and gray matter infarction cortical superfi bad luck (ie., A sign of the
insular ribbon), hipodensitas ganglia basalia (ie., Hipodensitas nuclei lentiformes), sign
hiperdensitas cerebral artery (middle cerebral artery, MCA), and sign Sylvian dot. In the
acute period (6-24 hours), change picture non-contrast CT scan due to ischemia becomes
increasingly clear. The distribution of blood vessels infarct also increasingly evident in this
phase. In the subacute period (1-7 days), there is an increase edema and mass effect which
causes a shift to the infarcted tissue lateral and vertical (in case of the infarcted area of large
blood vessels). Hipodensitas chronic infarction is characterized by a striking and reduced
mass effect on CT scan picture; the density of infarct area equals cerebrospinal fluid.

Keywords: ischemic stroke, hyperacute infarction, acute infarction, infarct subacute, chronic
infarction
ABSTRACT

Stroke is a leading cause of death worldwide. In the case of hyperacute ischemic

stroke (0-6 hours), CT scan is usually not sensitive in identifying cerebral infarction;
however, quite sensitive in identifying various forms of acute intracranial hemorrhage and
other macroscopic lesions contraindicate the use of thrombolytic therapy. Picture infarction
hyperacute on CT scan in the form of silting sulcus accompanied by the disappearance of
boundaries white matter and gray matter infarction cortical superfi bad luck (ie., A sign of the
insular ribbon), hipodensitas ganglia basalia (ie., Hipodensitas nuclei lentiformes), sign
hiperdensitas cerebral artery (middle cerebral artery, MCA), and sign Sylvian dot. In the
acute period (6-24 hours), change picture non-contrast CT scan due to ischemia becomes
increasingly clear. The distribution of blood vessels infarct also increasingly evident in this
phase. In the subacute period (1-7 days), there is an increase edema and mass effect which
causes a shift to the infarcted tissue lateral and vertical (in case of the infarcted area of large
blood vessels). Hipodensitas chronic infarction is characterized by a striking and reduced
mass effect on CT scan picture; the density of infarct area equals cerebrospinal fluid.

Keywords: ischemic stroke, hyperacute infarction, acute infarction, infarct subacute, chronic
infarction
 Daftar Isi
Kata Pengantar........................................................................................ i
Abstract.................................................................................................... ii
Abstrak..................................................................................................... iii
Daftar Isi................................................................................................... iv
BAB I. Pendahuluan
1.1.Latar Belakang................................................................. ...... 1
1.2.Tujuan...................................................................................... 2
1.3.Manfaat............................................................................ ...... 2
BAB II. Tinjauan Pustaka
2.1. Anatomi/Fisiologi............................................... .................. 3
2.2. Infark Cerebral
2.2.1. Definisi................................................................... 6
2.2.2. Epidemiologi.......................................................... 6
2.2.3. Etiologi............................................................. ...... 6
2.2.4. Gejala dan Tanda............................................. ...... 7
2.2.5. Patofisiologi/Patogenesa......................................... 8
2.2.6. Diagnosa
2.2.6.1. Anamnesa................................................ 9
2.2.6.2. Pemeriksaan Fisik.................................... 9
2.2.6.3. Pemeriksaan Penunjang........................... 10
2.2.7. Diagnosa Banding................................................... 13
2.2.8. Tatalaksana.............................................................. 14
2.2.9. Pencegahan............................................................ 14
2.2.10.Komplikasi............................................................ 14
2.2.11. Prognosa................................................................ 15
BAB III. Penutup
3.1. Kesimpulan ............................................................................ 16
3.2. Saran...................................................................................... 16
BAB IV. Daftar Pustaka.................................................................... 17