Journal Reading Radiology_clarissa Edit
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Transcript of Journal Reading Radiology_clarissa Edit
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PEMBIMBING: DR.MUNIR, SP.RAD.
PRESENTAN : CLARISSA TERTIA– 07120100009FK – UPH
KEPANITERAAN KLINIK BAGIAN ILMU RADIOLOGI
“MDCT Imaging Findings of Liver Cirrhosis: Spectrum of Hepatic and
Extrahepatic Abdominal Complications”
(Guillermo P. Sangster, Carlos H. Previgliano, Mathieu Nader, Elisa Chwoschtschinsky, and Maureen G. Heldmann)
Journal Reading
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Pendahuluan
Sirosis Hepatis: penyakit yang ditandai perubahan parenkim hati normal menjadi fibrosis yang ekstensif disertai regenerasi noduler
Sirosis Hepatis -> meningkatkan resiko HCC
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Manifestasi pada Hepar
Perubahan patologi: - fibrosis- distorsi nodular- perfusi yang abnormal
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Perubahan Fibrosis
Portal venous phaseUnenhanced CT
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Perubahan morfologi:1. Tahap awal :
- Hepatomegali- Pelebaran porta hepatis- Pembesaran fissura interlobaris- Ekspansi ruang perikolesistik
2. Tahap lanjut:Ukuran hepar mengecil (terutama alkoholik): segmen medial (IV) dari lobus kiri mengecil disertai dengan hipertrofi dari segmen lateral (II,III) -> “tongue-like appearance” -> kontur yang bernoduler dan heterogen
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Hepatic Steatosis
Sering pada alcohol-induced cirrhosisRespon hepatosit terhadap injury yang kronik
yang bersifat reversibelInfiltrasi dari fat yang difus dan uniform di
semua lobus heparAtenuasi rata-rata liver menjadi minimal 10
HU lebih kecil dari parenkim lien pada unenhanced CT
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Lesi Noduler Hepar
Nodul regeneratifNodul displastikHCC
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Nodul regeneratif
•Area dengan batas yang jelas pada parenkim hepar yang membesar akibat nekrosis dan perubahan sirkulasi
•Morfologik, dibagi 2:
1. Mikronodular: <3mm
2. Makronodular: >3mm
•Jika mengandung besi (siderotic nodul)-> hiperdense pada non-kontras CT
•Tidak enhance pada fase arterial-> isodense dengan parenkim sekitarnya pada fase vena -> susah dibedakan dengan hepar yang normal
Siderotic regenerative nodules
axial coronal
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Makronodular
Arterial phase CT ->multiple nodular isodense
Intraoperative
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Nodul displastik
Hepatosit dengan nodul displastik tanpa karakteristik keganasan
Berukuran 5-10mmBisa berlanjut menjadi HCC : peningkatan
progresif suplai arteri disertai dengan penurunan suplai vena porta
Nodul tampak lebih jelas setelah pemberian kontras pada fase awal arterial
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Nodul displastikNodul displastik HCCHCC
Perubahan keganasan pada venous phase CT
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HCC
Neoplasma ganas Lesi kecil : enhance homogeneouslyLesi besar: enhance heterogenously dengan
corak mosaik akibat nekrosis di dalam lesi80-90% -> highly vascular lesionKebanyakan memiliki kapsul fibrous yang
hipodense pada fase arterial hepatik dan enhance pada fase delayed
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Massa Soliter pada HCC
precontrast postcontrast
Delayed phase Delayed enhancement of capsule
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Massa dominan dengan lesi kecil (multicentric)
Arterial phase contrast
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Difus HCC
Focal intrahepatic biliary dilatation
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Penyebaran HCC ke vena porta (Portal Vein Thrombosis)
Filling defect
Small peripheral HCC
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Penyebaran HCC ke Inferior Vena Cava
Central filling defect
Large HCC
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Manifestasi pada Abdomen Extrahepatik
Hipertensi PortalAscitesSplenomegaliEdema difus intra dan retroperitonealPenebalan dinding usus halus dan gallbladder
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Hipertensi Portal
Tekanan porta melebihi 5-10mm Hg -> terbentuk sistem kolateralis -> darah mengalir menjauhi hepar menuju pembuluh darah sistemik yang memiliki tekanan yang lebih rendah
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Varises
Pemberian kontras IV -> penting untuk melihat alur struktur dari vena yang dilatasi
Coronary Varices -> vena gastrika kolateralis sinistra (80%) -> 5-6mm pada CT : hipertensi portal
Varises esofagus dan paraesofagusCaput medusae : dari umbilikus
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Varises esofagus dan paraesofagus
axial sagital
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Vena kolateralis paraumbilikal
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Caput Medusae
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Varises Retrogastric
Varises retrogastrik -> karena gastrorenal shunt
Varises retrogastrik -> karena gastrorenal shunt
Retrogastric varices
Gastrorenal shunt
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Thrombosis Vena Porta
Trombus di dalam lumen -> hipodense sentral dengan pemberian kontras
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Trombosis vena porta Kronik
Axial Coronal
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Splenomegali
9-12% terdapat fokus yang terdeposisi oleh hemosiderin di dalam lien -> “Gamna- Gandy bodies” -> bisa hipo-hiperdense pada CT tergantung deposisi sekunder dari kalsium
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Splenomegali
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Penebalan dinding Gastrointestinal•64%•Karena hipoproteinemia akibat sirosis hepatis•Paling sering : Jejenum dan kolon ascendens•IV kontras: homogen enhancement
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Penebalan difusa dinding Gallbladder
Penyebab:- peningkatan tekanan vena porta- penurunan tekanan osmotik intravaskular- hipoproteinemia
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Ascites -> komplikasi tersering pada sirosis
•Akumulasi cairan di dalam rongga peritoneal
•Penyebab: permeabilitas dan tekanan onkotik
•Karakteristik cairan:transudat kuning dengan total konsentrasi protein <2.5g/dL dan sedikit sel-sel.
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Kesimpulan
Sirosis hepatis merupakan penyakit dengan berbagai etiologi yang insidennya semakin meningkat.
HCC merupakan komplikasi yang mematikan : 5% setelah 5 tahun terinfeksi hepatitis yang menyebabkan sirosis.
CT dengan triple phases pada hepar -> penting untuk mendeteksi HCC kecil.
Komplikasi extrahepatik abdomen->untuk terapi
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Terima Kasih