Bài giảng CT bệnh lý gan

Multiple hepatomas

 Multiple hepatomas

 Embolization coils in

gastroduodenal artery

prior to therasphere

embolizationhepatoma

 Large hepatoma  Portal vein thrombosishepatoma

 Large hepatoma  Lung metastasishepatoma

 Large hepatoma with

portal vein thrombosis

 Cavernous

transformation of portal

veinhepatoma

 Hepatoma adjacent to

thrombosed portal vein

 Gallium 67 c

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Allen J. Cohen, Ph.D., M.D. Department of Radiological Sciences University of California, Irvine Liver, Biliary Tree,Gallbladder U gan lành tính 1. U tuyến (Hepatic adenoma) 2. Tăng sản thể nốt (Focal nodular hyperplasia) 3. Regenerating nodule 4. Nang (Cysts) 5. U tuyến đường mật (Biliary cystadenoma) 6. U máu (Hemangioma) 7. U mỡ (Lipoma) 8. Tụ máu (Hematoma) 9. Áp xe (Abscess) 10. Nhiễm mỡ vùng (Focal Fat) U gan ác tính 1. Ung thư tế bào gan (Hepatocellular carcinoma) 2. Ung thư tế bào xơ dẹt (Fibrolamellar HCG) 3. Ung thư nguyên bào gan (Hepatoblastoma) 4. Ung thư đường mật (Cholangiocarcinoma) 5. Nang ung thư (Cystadenocarcinoma) 6. U máu ác tính (Angiosarcoma) 7. U biểu mô mạch máu (Hemangioendothelioma) 8. U hạch nguyên phát (Primary lymphoma) 9. Di căn (Metastasis) Chụp cắt lớp vi tính Computed Tomography: 1. Đánh giá giai đoạn và theo dõi di căn. 2. Chẩn đoán các u nguyên phát: hepatoma, adenoma, FNH, cholangioCa. 3. Áp xe. 4. Chấn thương bụng kín. 5. U hạ sườn phải. 6. Bệnh gan lan tỏa:Budd-Chiari, hemochromatosis. Siêu âm: 1. Nang và tổn thương đặc. 2. Siêu âm Doppler: tưới máu, TMC. 3. Đường mật và túi mật +++. 4. U hạ sườn phải. 5. Tìm tổn thương trong phẫu thuật. Các phương pháp chẩn đoán hình ảnh: Y học hạt nhân 1. U máu. 2. U gan. 3. Lưu thông mật. 4. Chức năng gan. Chụp cộng hưởng từ hạt nhân (MAGNETIC RESONANCE IMAGING) 1. U máu 2. Nang. 3. Nhiễm mỡ vùng. 4. U gan: nguyên phát hay thứ phát. Các phương pháp chẩn đoán hình ảnh: I. Nang gan Bẩm sinh, sau nhiễm trùng, sau chấn thương, nhiễm ký sinh trùng. Bẩm sinh-hay gặp. CT: Không ngấm thuốc, thành mỏng và đều. Nhiều nang gan 40% . Nang nhỏ < 1 cm khó phát hiện bằng CT hay US. Chẩn đoán phân biệt: di căn gan, áp xe nhỏ (metastasis, micro-abscess). Nang gan đơn thuần  Bẩm sinh Nhiều nang gan  Trên CT nghĩ đến di căn Nhiều nang gan  Gan thận đa nang Áp xe gan  A míp Nguồn: Máu, đường mật, sau chấn thương, sau phẫu thuật CT: Giảm tỷ trọng, ngấm thuốc vỏ US: Giảm âm, khí bên trong A míp: Lớn, bên phải Sán chó (Echinococcal): vách, vôi hóa vỏ trứng++ Nấm: Nhiều, nhỏ Nhiễm trùng mủ: đặc, lớn Áp xe a míp  Khí bên trong  Thuốc cản quang vòa ổ áp xe do thông với tá tràng Sán chó Echinococcal abscess  Membranes within cyst  E. granulosis Echinococcal abscess  MRI-Large liver abscess-daughter cysts Áp xe do nấm  Ổ áp xe nhỏ được phát hiện vớ cửa sổ hẹp Áp xe gan  Áp xe lách do nấm  Áp xe do vi khuẩn Viêm gan do ban xuất huyết Sau bị mèo cào U tuyến tế bào gan  Máu tụ dưới bao gan do vỡ adenoma 1. Dạng nang, vỏ xơ 2. Phụ nữ trẻ, thuốc 3. Đau do u, chảy máu 4. Tiền ung thư 5. Chẩn đoán: CT U tuyến tế bào gan  Ngấm thì ĐM Tăng sản thể nốt (Focal nodular hyperplasia)  Enhances in arterial phase  Becomes isodense in portal venous phase Focal Nodular Hyperplasia  Pedunculated FNH with central scar- remnant of AVM Focal nodular hyperplasia  Central scar  Tc sulfur colloid avid Focal nodular hyperplasia  Focal nodular hyperplasia  Central scar Regenerating Nodules  Cirrhotic liver-spontaneous spleno-renal shunt Hemangioma 1. Occurrence – 10% of adults; F>M. 2. Thin-walled vascular spaces without smooth muscle. 3. Slow circulation. 4. Hemorrhage – rare. Diagnosis: 1. Ultrasound: round echogenic focus without hypoechoic halo. 2. CT: precontrast – hypodense mass. contrast – rim enhancement initially. delay – centripetal filling in. 3. Tc-labeled RBCs for lesions > 2 cm. 4. T2-weighted MR for lesions < 2cm. hemangioma  Hemangioma mimicking a liver abscess  Classic echogenic ultrasound finding of hemangioma hemangioma  Globular peripheral enhancement  Lesion fills in from periphery hemangioma  Large hemangiomas may not be echogenic  Globular peripheral enhancement hemangioma  Contrast filling in from periphery hemangioma  Photopenic on Tc sulfur colloid scan  Lesion fills in on Tc tagged RBC scan hemangioma  Hemangioma caused feeling of early satiety Thrombosed hemangioma  Thrombosed hemangioma thought to be hepatoma  CT of thrombosed hemangioma Thrombosed hemangioma  Same patient as before-5 years earlier  Large thrombosed hemangioma Giant Hemangioma  Interrupted globular enhancement of periphery is characterisic Multiple Hemangiomas  Interrupted globular enhancement of periphery is characterisic Hepatocellular carcinoma 1. Vascular malignant tumor – solitary or multifocal. 2. Tumor thrombus, hemorrhage, metastases. 3. Elevated alpha-fetoprotein ( 80% of patients.) 4. Associated with hepatitis B, hepatitis C, alcohol Diagnosis: 1. CT: inhomogeneous enhancement, delayed isoattenuation fibrous capsule – may mimic adenoma. 2. NM: Gallium uptake 90%. Hepatoma  Enhancing lesion in arterial phase in lateral segment of left lobe. Hepatoma  SPECT/CT scan shows tumor to be Gallium avid and sulfur colloid cold hepatoma  Faintly seen on precontrast phase  Very subtle arterial enhancement hepatoma  Best seen on portal venous phase (not common)  Different patient- multiple small hepatomas hepatoma  Same patient – other small hepatomas Tiny Hepatoma  Examination obtained with cardiac gating Multiple hepatomas  Multiple hepatomas  Embolization coils in gastroduodenal artery prior to therasphere embolization hepatoma  Large hepatoma  Portal vein thrombosis hepatoma  Large hepatoma  Lung metastasis hepatoma  Large hepatoma with portal vein thrombosis  Cavernous transformation of portal vein hepatoma  Hepatoma adjacent to thrombosed portal vein  Gallium 67 citrate avid tumor hepatoma  Recurrent treated hepatoma  Portal vein thrombosis hepatoma  Superior mesenteric vein thrombosis  Infarcted colon- pneumatosis intestinalis hepatoma  Hepatoma  6 months later after treatment with Radiofrequency Ablation hepatoma  Yttrium microsphere embolization of right lobe hepatoma: large tumor has become necrotic,  new hepatomas have appeared in left lobe Hepatoma chemoembolization 50 mg cisplatin, 50 mg doxyrubicin, Embogold microparticles 300-500 microns Suspected hepatoma  Hep C positive and rising alpha feto protein  Lesion missed on CT and MRI Suspected hepatoma  Liver-Spleen scan suggested lesion  Hepatoma detected by CT 6 months later hepatoma  Pedunculated hepatoma Fibrolamellar Hepatoma  Young non cirrhotic patient, normal AFP Hepatic lymphoma  Multiple liver lesions  Obstructing left kidney  Destroying verterbral body Liver malignancies  Lymphoma  Cholangiocarcinoma Cholangiocarcinoma  Tumor occupies lateral segment of left lobe  Metastases in right lobe Hepatic metastases 1. Colon, breast, lung, pancreas – hepatic artery supply. 2. CT: hyperattenuating, hypoattenuating or hypoattenuating with rim enhancement. Hepatic metastases  metastasis in fatty liver metastatic colon Ca Hepatic Metastases Initial presentation ,three months,15 months,18 months Hepatic Metastases  Colon carcinoma metastatic to lliver and lungs Hepatic Metastases  Metastatic breast cancer-note sclerotic veterbral metastasis and absent left breast Liver segments Segment characterization  Liver metastasis  Segmental anatomy better depicted on MRI –orthogonal planes than single slice CT. multislice CT may be best Liver lesion diagnosis  CT arterial portography metastases  CT arterial portography- thrombosed right portal vein Carcinoid metastases  Cystic carcinoid metastases-unusual  Classic arterial enhancement of carcinoid metastasis Carcinoid metastases Arterial phase images, narrow and wide windows Portal venous phase imaging Carcinoid metastases-after treatment with octreotide Less vascularity in Arterial phase Partially necrotic in portal venous phase Fatty liver  Diffusely fatty liver DIFFUSE HEPATIC DISEASE 1. Fatty infiltration – focal diffuse. Chemotherapy, hyperalimentation, alcohol, obesity, diabetes, hyper- triglycerides. CT: normal liver 5-10 Hounsfield units > spleen on noncontrast scan 2. Cirrhosis – alcoholism, viral hepatitis, cryptogenic cirrhosis, sclerosing cholangitis. 1. Sequella of chemotherapy, random. 2. CT: normal vascular pattern. 3. MR: fat-suppression. Focal fatty liver Focal fatty liver  Normal vascularity preserved  Focal Fat- T1 Fat Sat Focal Fatty Liver  Suspected mass on ultrasound  Focal Fatty Liver on CT Focal fatty liver  Focal normal liver in sea of fatty liver-two cases cirrhosis  Regenerating nodules  Ascites  Recanalized periumbilical vein  Caput Medusa cirrhosis  Recanalized periumbillical vein  Partial thrombosis of portal vein  Coronal reformation cirrhosis  Giant paraesophageal varices and coronary vein, cavernous transformation of portal vein,  Patient with cirrhosis and hepatoma Cirrhosis-hepatofugal flow Diffuse hepatic disease  Dense liver- hemochromatosis Hemochromatosis – congenital, iron overload. Transfusional hemosiderosis – anemia treatment. CT non-contrast – normal 50-60 HU. Abnormal 70-100 HU. Diffuse hepatic disease  Post transfusional hemosiderosis in child with leukemia Budd-Chiari malformation  Suspected gastric leiomyosarcoma DIFFUSE HEPATIC DISEASE Budd-Chiari syndrome: Chronic hepatic vein congestion. Tumor, web, phlebitis, blood dyscrasia – thrombus. CT: Hepatomegaly – central, caudate lobe enhancement. Hypodense periphery. Central veins not seen. Budd-Chiari Syndrome  Massively enlarged caudate lobe-thought to be a hepatoma Budd-Chiari Syndrome  Portal venous flow  No hepatic venous flow Budd-Chiari Syndrome  Occluded hepatic veins  Post biopsy biloma in another patient with Budd- Chiari syndrome Portal Vein Thrombosis Portal vein thrombosis with cavernous transformation Post transplant evaluation  Hepatic artery patency Intraoperative ultrasound 1. Focal masses 2. Transplant vascularity Intraoperative ultrasound  Needle localization  Probe localization BILIARY TREE CONGENITAL ABNORMALITIES 1.Choledochal cyst – marked extra-hepatic dilation, minimal to no intrahepatic dilation. Risk: stones, cholangiocarcinoma. 2. Choledochocele – focal dilation of distal CBD. 3. Caroli’s disease – segmental dilatation of intrahepatic bile ducts associated with renal cysts, MSK. Congenital abnormalities  Choledochal cyst  Choledochocele Congenital abnormalities  Choledocal diverticula  Caroli’s disease Choledochal cyst  CT-Choledochal cyst Choledochal cyst  Ultrasound  MRI Choledochal cyst  CT Hepatobiliary scan Choledochal cyst  US- thick wall cyst  6 months later - metastatic cholangiocarcinoma Biliary tree  Hamartoma of bile duct Benign stricture – gradual tapering Malignant stricture – abrupt cutoff Inflammatory 1. Acute cholangitis – biliary gas, wall enhancement 2. Sclerosing cholangitis – association – UC, Crohn disease, retroperitoneal fibrosis. Extra (95%) & intrahepatic strictures. Beaded ducts. Focal dilatation – suspect cholangiocarcinoma. 3. Recurrent pyogenic cholangiohepatitis Marked extrahepatic, intrahepatic duct dilatation. Numerous stones – cast of biliary tree 4. Choledocholithiasis. Pericholecystic abscesses  Pericholangitic abscesses  Different patient -AIDS- abscesses-liver,spleen AIDS cholangitis  Beaded ducts  AIDS gallbladder AIDS cholangitis  AIDS gallbladder  CMV cholecystitis AIDS cholangitis  Papillary stenosis-AIDS cholangitis Cholangitis  Sclerosing cholangitis  Periportal nodes- primary bilary cirrhosis recurrent pyogenic cholangiohepatitis  Calcified soft intrahepatic stone  Vietnamese Buddhist monk with right upper quadrant pain Recurrent cholangiohepatitis  Soft common duct stone  Stone in left duct Common bile duct stone  Subtle distal common bile duct stone-filling of intrahepatic radicles, no tapering at ampulla  After stone removed Common bile duct  Ischemic stricture  CBD entering diverticulum Common bile duct obstruction  Tension from T-Tube  Different patient- jaundiced-dilated intrahepatic bile ducts Common bile duct  No excretion into bile duct on Tc hepatobiliary scan  Common duct stone Common bile duct obstruction  Dilated intrahepatic bile ducts  stone in distal CBD cholangiograms  Ducts of Luschka-bile leak  pancreatitis Bilary tree: neoplastic disease 1. Cholangiocarcinoma – Klatskin, intrahepatic, extrahepatic. 2. Metastatic to porta hepatis – lymphoma, ovarian, colon, gallbladder, pancreas, stomach. CHOLANGIOCARCINOMA 1. Klatskin tumor a. CT detection of mass difficult. b. ERCP. 2. Peripheral – may be multifocal. Sclerosing cholangitis  ERCP  Same patient-7 years later-cholangiocarcinoma cholangiocarcinoma  Klatzkin tumor at confluence of ducts cholangiocarcinoma  ERCP showing stented obstructing stricture cholangiocarcinoma  Dilated ducts with atrophy  ERCP showing stricture cholangiocarcinoma  Obstruction at porta hepatis  Stented tumor cholangiocarcinoma  Dilated intrahepatic bile ducts  Delayed enhancement of tumor Cholangiocarcinoma  Intraductal tumor- thought to be stones or clot  6 months later, tumor enlarged, obstructing ducts cholangiograms  cholangiocarcinoma obstructing common bile duct  Pancreatic tumor obstructing common bile duct Ovarian Carcinoma metastatic to porta hepatis Biliary dilatation, masses at porta, retroperitoneal adenopathy, left ovarian cystadenocarcinoma MRCP  MRCP-stone at ampulla  MRCP-common duct stones MRCP  Low insertion of cystic duct not appreciated on previous CT scan Gallbladder  cholesterol polyps Oral cholecystograms  Polyps  hypercontractility gallbladder  Septated gallbladder gallbladder  CT - adenomyosis  US - adenomyosis gallstone  No stone seen on ultrasound  Gallstone seen on CT Gallstones  Fissured Cholesterol Stones cholecystitis  right portal vein thrombosis-THAD-transient hepatic attenuation difference-right lobe enhances before left lobe  Cholecystitis as cause of right portal vein thrombosis Acute cholecystitis  Calcified gallstones  Perforated gallbladder with pericholecystic inflammation Acute emphysematous cholecystitis  Usually diabetic patients, need emergency surgery Gallbladder Cancer  6.500 Deaths/year in U.S.  3:1 Female:male Radiology:  Mass replacing gallbladder 40-65%  Focal/diffuse wall thickening 20-30%  Intraluminal mass 15-25%  Gallstones in 70-80%  Porcelain gallbladder – 25% risk of cancer SPREAD OF GALLBLADDER CANCER 1. Extension into liver. 2. Extension into subhepatic space. 3. Extension into bowel. 4. Extension to extrahepatic bile duct. 5. Lymphatic. 6. Hematogenous Gallbladder Cancer  Stones on ultrasound  Tumor growing into liver Jaundiced patient  Dilated intrahepatic ducts  Nonvisualization of gallbladder Jaundiced patient  Obstruction at porta hepatis on ERCP  Subtle gallbladder cancer Gallbladder carcinoma  Gallbladder cancer growing into liver  Perforated gallbladder cancer with pericholecystic abscess Gallbladder carcinoma  right portal vein thrombosis-THAD- transient hepatic attenuation difference-right lobe enhances before left lobe Gallbladder cancer as cause of right portal vein thrombosis Leiomyosarcoma of gallbladder Ultrasound-anechoic mass CT- homogeneous mass Leiomyosarcoma of gallbladder  Post therapy- suspected metastasis  Focal normal liver anterior to fatty liver Patient with vomiting  Large gas collection in right upper quadrant  MR-gallstone in empyema of gallbladder obstructing stomach, patient also has cystic lesions of kidneys-tuberous sclerosis Quiz Case-elderly patient with severe abdominal pain Quiz Case  CT scan two years earlier Perforated Gallbladder  Gallstones are now in peritoneal cavity

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