25

DAVID SUTTON

DAVID SUTTON PICTURES

DR. Muhammad Bin Zulfiqar PGR-FCPS III SIMS/SHL

• Fig. 25.1 Liver of normal size and shape. Hepatogram following coeliac angiogram. Lower right lobe related to hepatic flexure (single arrow). Caudate lobe to duodenum (facing arrows), left lobe to gastric fundus (arrowheads).

• Fig. 25.2 Indirect portal venogram. Note large Reidel's lobe (segment VI) projecting downwards on right.

• Fig. 25.3 Multiple large-bowel metastases causing gross hepatomegaly. Elevated right hemidiaphragm, depressed right kidney (thin arrows) and transverse colon (thick arrows).

• Fig. 25.4 (A) Patient with carcinoma of the stomach. Right hemidiaphragm normal preoperatively. (B) The same patient 3 months later. Elevation of right hemidiaphragm with slight humping medially is a highly significant abnormality. Liver biopsy: metastatic adenocarcinoma.

• Fig. 25.5 Contrast enhanced CT. Hepatosplenomegaly. Dilated bile ducts containing many stones. Congenital hepatic fibrosis with secondary portal hypertension.

• Fig. 25.6 Selective hepatic arteriogram. Multiple small, dense, welldefined stains arise from normal-sized hepatic arteries, and persist over

• Fig. 25.7 Unenhanced CT. Irregular anterior liver border indicates cirrhosis. Overall increased density is due to haemochromatosis. Intra-arterial Lipiodol has been taken up by hepatomas. Note ascites.

• Fig. 25.8 (A) Chest film of 28-year-old woman with fever, reported as normal. (B) Repeat film after 1 week shows marked localised hump of diaphragm (arrow). Aspiration: amoebic abscess. The shape of the abnormal diaphragm contour does not help in distinguishing an inflammatory from a neoplastic cause. However, a change over days favours an abscess, and over months a slower-growing lesion such as a hepatic cyst or tumour.

• Fig. 25.9 Left subphrenic abscess 12 days after perforated gastric ulcer. Barium has shown the stomach to be compressed and displaced medially by the abscess, with fluid level. High hemidiaphragm with fluid above.

• Fig. 25.10 CT in patient with high fever after a foreign holiday. The semi liquid mass in the right lobe of the liver has concentric walls (compressed liver tissue) and a central speck of gas. An abscess can be diagnosed with certainty (aspirate:amoebae).

• Fig. 25.11 (A) Multiple hepatic calcifications are typical of phleboliths: haemangiomas. (B) Typical egg-shell calcification: echinococcal cyst.

• Fig. 25.12 Faint amorphous calcification within liver. Biopsy: primary liver cancer.

• Fig. 25.13 Multiple areas of fluffy calcification in a patient with metastases from carcinoma of the thyroid. All the signs of hepatomegaly are present.

• Fig. 25.14 CT scan of high right lobe of liver. A small rim of calcification lies adjacent to a cyst, suggesting that it is hydatid. Strongly positive hydatid serology.

• Fig. 25.15 Non-enhanced CT scan of liver in haemochromatosis. Portal vessels appear as strikingly low-density channels within the denser iron loaded liver (liver density 90 HU). Splenomegaly.

• Fig. 25.16 Portal pyaemia following mesenteric artery infarction. Gas is present in peripheral branches of the portal vein.

• Fig. 25.17 46-year-old man. There is partial interposition of colon between the liver and the right hemidiaphragm (large arrow). Note normal spleen size and its relationships to stomach and colon (small arrows).

• Fig. 25.18 Unenhanced CT in alcoholic. Low-density liver is due to excess fat, although segment 1 around the inferior vena cava is spared. Note calcific pancreatitis.

• Fig. 25.19 DSA. Normal coeliac angiogram. The hepatic arteries are regular.

• Fig. 25.20 DSA. Selective hepatic arteriogram in cirrhosis. Note corkscrewed arteries in a small liver.

• Fig. 25.21 Selective hepatic angiogram (DSA). Arteries feeding a vascular liver tumour communicate in this early frame with the portal vein, which fills retrogradely and contains tumour thrombus. This appearance is diagnostic of hepatocellular cancer (HCC).

• Fig. 25.22 Hepatic arteriogram performed because of palpable right lobe of liver. A large localised vascular tumour mass is seen in Reidel's lobe. Both liver adenoma and well-defined HCC (hepatoma) could have this appearance. A vascular metastasis does not usually have such large feeding arteries.

• Fig. 25.23 Osler-Rendu-Weber syndrome (hereditary haemorrhagic telangiectasia). Selective hepatic arteriogram. Grossly dilated hepatic arteries, which shunted early to hepatic veins. No tumour circulation.

• Fig. 25.24 DSA in a patient with multiple metastases who developed haemoperitoneum after liver biopsy. (A) Hepatic arteries stretched around avascular masses. A bead of contrast laterally (arrow)-bleeding site. (B) Bleed has ceased after selective embolisation with polyvinyl alcohol particles.

• Fig. 25.25 (A) 45-year-old woman who had taken the contraceptive pill for 16 years. Vascular adenomas in the liver (biopsy proof). (B) Angiogram postembolisation with dextrose, Gelfoam and absolute alcohol. No tumour circulation. No further therapy. Asymptomatic 14 months later. This is an example of embolisation as an alternative to surgery.

• Fig. 25.26 (A) Boy aged 5 with a rapidly enlarging liver and highly vascular unusual 'tumour' in the left lobe of the liver. Embolised prior to surgery. (B) Postembolisation angiogram. Note wire coil in mouth of the left hepatic artery (right hepatic originated from superior mesenteric). This is an example of embolisation as an aid to surgery.

• Fig. 25.27 DSA after Lipiodol has outlined multiple vascular malignant tumours. Radioactive Iodine-131 has been incorporated in the injection. Note the presence of a biliary stent.

• Fig. 25.28 CT portogram. The avascular filling defect high in the right lobe posteriorly abuts the inferior vena cava and compressed right hepatic veins, while the remainder of the (normal) liver enhances. Diagnosis: solitary large-bowel metastasis, predicted as suitable for resection.

• Fig. 25.29 (A) Hepatic arterial study. Both lobes are large and contain numerous vascular carcinoid tumour metastases. Patient highly symptomatic. (B) Study after embolisation with polyvinyl alcohol, dextrose and Gelfoam. Patient alive 10 years later.

• Fig. 25.30 Multiple liver metastases high right lobe. Biopsy site carefully selected, and tissue obtained from viable periphery of lesion: metastases from haemangiopericytoma.

• Fig. 25.31 Barium meal. Indentation on gastric mucosa (arrows) was due to a splenunculus

• Fig. 25.32 Gross splenomegaly in the Banti syndrome. Note elevation of left hemidiaphragm.

• Fig. 25.33 89-year-old woman, plain X-ray of abdomen. Tortuous parallel-line calcification in splenic artery.

• Fig. 25.34 31-year-old Arab man. Known previous tuberculosis affecting spleen and left kidney; both shows areas of calcification.

• Fig. 25.35 39-year-old woman. Calcified non-parasitic cyst in spleen.

• Fig. 25.36 19mTc-colloid scan in patient with severe left hypochondria pain. Small infracting spleen.

• Fig. 25.37 CT. Multiple metastases in spleen from carcinoma of thyroid.

• Fig. 25.38 (A) Enhanced CT. Triangular non-enhancing defect in spleen after trauma (arrow). Subcapsular hepatic fluid (arrowheads). (B) Another patient. Spleen pulped from major trauma. Enhanced CT. Arrow indicates only viable tissue. Note dense fluid in peritoneum (blood).

• Fig. 25.39 Investigation of bleeding in suspected portal hypertension.

• Fig. 25.40 (A) Splenic arteriogram (digital subtraction). Normal arteries and non-enlarged spleen. (B) Venous phase. Normal splenic and portal veins, with no filling of tributaries or collaterals.

• Fig. 25.41 Coeliac angiogram in portal hypertension. Sparse liver arteries. Enlarged tortuous splenic artery with aneurysms on main trunk and divisions. Intrasplenic branches stretched within grossly enlarged spleen which has vertical axis (cf. Fig. 25.40A).

• Fig. 25.42 (A) DSA. Venous phase superior mesenteric artery injection. Portal vein widely patent. Liver tiny in size-ascites suspected. Note filling of left gastric (coronary) vein thence gastric and oesophageal varices. (B) Duplex Doppler ultrasound. Ascites is confirmed. Portal vein flow is 24 cm/s.

• Fig. 25.43 Reformat of spiral CT axial image to show portal vein and gastric varices in coronal projection.

• Fig. 25.44 Hepatic phlebogram. Occlusal balloon method. Normal major and minor veins. Occlusion pressure normal at 6 mmHg.

• Fig. 25.45 (A) Hepatic phlebogram. Occlusal balloon method. Irregular hepatic vein radicles and bizarre sinusoidogram. Corrected pressure 16 mmHg: cirrhosis. (B) DSA hepatic venogram. The right vein occludes close to site of its caval entry. Contrast outlines 'spider's web' of new venous collaterals. Budd-Chiari syndrome.

• Fig. 25.46 Transjugular liver biopsy. Cutting needle introduced via right hepatic vein.

• Fig. 25.47 DSA of superior mesenteric artery, assessing effect on flow of various drugs. Fr 8 catheter houses Fr 3 micro tip disposable Doppler catheter (arrow). Note graduated markers on right (4-10 mm).

• Fig. 25.48 TIPS procedure (DSA). (A) Phlebogram shows right hepatic vein occlusion near its caval junction. Note reflux via spider's web network into portal vein, thence into left gastric vein (patient had acutely bleeding varices). (B) TIPS completed. A 12 mm diameter metal stent has relieved the portal hypertension. (C) Follow-up Doppler ultrasound. Turbulent flow enters the stent.

• Fig. 25.48 TIPS procedure (DSA). (A) Phlebogram shows right hepatic vein occlusion near its caval junction. Note reflux via spider's web network into portal vein, thence into left gastric vein (patient had acutely bleeding varices). (B) TIPS completed. A 12 mm diameter metal stent has relieved the portal hypertension. (C) Follow-up Doppler ultrasound. Turbulent flow enters the stent.

• Fig. 25.49 (A, B) Unenhanced CT showing hepatic and portal veins. (C, D) Enhanced study of these veins.

• Fig. 25.50 Non-enhanced CT. Fatty infiltration of liver, with focal sparing and mild hypertrophy of caudate lobe in cirrhosis. The small arrowed defect is a hepatoma.

• Fig. 25.52 Normal study. Curved plane reformation from a contrast enhanced spiral scan of the upper abdomen, demonstrating the splenic and portal veins.

• Fig. 25.53 (A) Non-enhanced scan shows poorly defined low-density mass-hepatoma. (B) Dynamic enhanced scan. Arterial phase shows greater enhancement in the defect than in surrounding liver: vascular hepatoma. (C) Delayed postcontrast venous phase scan shows persistent parenchymal density but loss of enhancement in the hepatoma, increasing its conspicuousness. (D) 10 days post-Lipiodol angiogram shows strong Lipiodol staining of the tumour. (E) CT at another level (post-Lipiodol) shows a satellite lesion in the left lobe of the liver (segment IV) (arrow) not seen on earlier scans.

• Fig. 25.53 (A) Non-enhanced scan shows poorly defined low-density mass-hepatoma. (B) Dynamic enhanced scan. Arterial phase shows greater enhancement in the defect than in surrounding liver: vascular hepatoma. (C) Delayed postcontrast venous phase scan shows persistent parenchymal density but loss of enhancement in the hepatoma, increasing its conspicuousness. (D) 10 days post-Lipiodol angiogram shows strong Lipiodol staining of the tumour. (E) CT at another level (post-Lipiodol) shows a satellite lesion in the left lobe of the liver (segment IV) (arrow) not seen on earlier scans.

• Fig. 25.53 (A) Non-enhanced scan shows poorly defined low-density mass-hepatoma. (B) Dynamic enhanced scan. Arterial phase shows greater enhancement in the defect than in surrounding liver: vascular hepatoma. (C) Delayed postcontrast venous phase scan shows persistent parenchymal density but loss of enhancement in the hepatoma, increasing its conspicuousness. (D) 10 days post-Lipiodol angiogram shows strong Lipiodol staining of the tumour. (E) CT at another level (post-Lipiodol) shows a satellite lesion in the left lobe of the liver (segment IV) (arrow) not seen on earlier scans.

• Fig. 25.54 (A, B) Patchy irregular enhancement of the hepatic parenchyma due to altered portal blood flow in cirrhosis with portal hypertension. Recanalisation of the umbilical vein in the falciform ligament is arrowed.

• Fig. 25.55 CT i n Budd-Chiari syndrome. Large oedematous liver, with huge caudate lobe. No hepatic vein radicles. Collateral veins in falciform ligament. Ascites.

• Fig. 25.56 Klatskin tumour of the left hepatic duct resulting in marked atrophy of the left lobe of the liver (asterisk). Some dilated right lobe ducts are evident, a percutaneous biliary drain is in situ.

• Fig. 25.57 (A) Arterial phase CT. Numerous metastases with ring enhancement. (B) Scan in equilibrium phase shows lesions are isodense with normal liver. They would be missed with slow scanning techniques. Biopsy: adenocarcinoma.

• Fig. 25.58 Spiral scan through the liver during contrast injection into the superior mesenteric artery. Large solitary non-enhancing metastatic lesion demonstrated in the left lobe of the liver (segment IV). (Courtesy of Dr N. Chalmers.)

• Fig. 25.59 Hepatic haemangioma. This is a characteristic site. (A) Unenhanced scan shows a mass of identical attenuation to that of the IVC. (B) During dynamic contrast enhancement, the periphery of the lesion takes up pools of contrast. (C) On delayed postcontrast scans the enhancement travels centripetally into the lesion.

• Fig. 25.60 Enhanced CT. Large vascular lesion in right lobe has a central scar: focal nodular hyperplasia. Other lesions. Note fatty liver.

• Fig. 25.61 Unenhanced CT. Hepatomegaly. Polycystic hepatic and renal disease.

• Fig. 25.62 CT. Small peripheral 'cyst' in right lobe is indeterminate. The nature is sometimes only clarified on follow-up.

• Fig. 25.63 CT. Hepatic abscess. The thick peripheral onion ring in the postcontrast scan (right) is typical.

• Fig. 25.64 CT. Small peripheral 'cyst' in right lobe is indeterminate. The (B) Major trauma. Non-enhancing cleavage area in right lobe is nonviable. nature is sometimes only clarified on follow-up. Right hepatic vein intact.

• Fig. 25.65 Regional liver function shown by 99 -Tc-IDA: shortly after auxiliary liver transplantation (A), the transplant liver (T) occupying the normal position of the right lobe provides virtually the whole of the patient's liver function. Nine months later (B) the patient's own left lobe (L) has regenerated and the transplant has been allowed to undergo rejection and atrophy.

• Fig. 25.66 Bile leak following liver trauma. Contrast-enhanced CT (A) showed a subcapsular fluid collection (asterisks) with segmental ischaemia (isch) but surgical exploration found no injury to the extrahepatic ducts. 99mTc-IDA scintigraphy (B) showed normal extrahepatic bile ducts (arrow) but leakage of bile from damaged intrahepatic ducts forming a subcapsular collection (asterisks).

• Fig. 25.67 Focal nodular hyperplasia. T,-weighted MRI (A) shows a large mass in the left lobe with typical morphology for FNH. (B) Scintigraphy with 99 'Tc-colloid (left) shows that the mass exhibits at least as much reticuloendothelial cell activity as the normal liver in the right lobe, while 99 mTc-IDA scintigraphy (right) shows active hepatocyte function with prolonged retention of tracer in the area of FNH.

• Fig. 25.68 Focal nodular hyperplasia. Gadolinium-enhanced T,-weighted MRI (A) shows a highly vascularised lesion in the right lobe. SPECT imaging after 99mTc-IDA (B) shows prolonged retention of the tracer in the abnormal area. The focus of activity anteromedial to the mass in (B) represents the confluence of the hepatic ducts and common duct.

• Fig. 25.69 Somatostatin receptor scintigraphy (SRS) in a patient with multiple liver metastases from pancreatic gastrinoma.

• Fig. 25.70 Small liver lesions shown by SRS in a patient with metastatic carcinoid. SPIO-enhanced MRI (A) shows a 1 cm lesion in the periphery of the right lobe (arrow). SRS (B) shows multiple small lesions against a background of normal activity in adjacent liver.

• Fig. 25.71 Carcinoid metastases presenting as a solitary liver lesion (arrow) on CT (A), with neuroendocrine activity shown by positive SRS (B). Note also an unsuspected lung metastasis shown on SRS (arrow).

• Fig. 25.72 99"Tc-colloid imaging in a patient with two unidentified rounded nodules in the left upper quadrant several years after splenectomy: focal uptake confirms the presence of splenunculi.

• Fig. 25.73 11mTc-colloid study following splenectomy for trauma. Fragments of splenic tissue entering into the omentum at surgery are now shown to be viable and functioning (liver uptake shielded on this image).

• Fig. 25.74 (A) Interrogation of the porta hepatis, using a 2.5 MHz probe, failed to reveal normal flow within the portal vein. (B) Following intravenous administration of ultrasound contrast medium (Levovist), reverse flow is now readily seen in the portal vein using the same settings as in (A).

• Fig. 25.75 Oblique intercostal scan in the right upper quadrant of the liver demonstrates forward flow (encoded red) in the portal vein. The hepatic artery is seen as a small focus of colour flow (small arrowhead) lying between the portal vein and bile duct (large arrowhead).

• Fig. 25.76 (A) Oblique intercostal scan demonstrates flow in the hepatic artery but no flow within the portal vein. (B) Scanning in the same position but with a lower PRF flow is now demonstrated within the portal vein.

• Fig. 25.77 Portal vein radicals have reflective walls (arrow) in contrast to the poorly reflective walls of hepatic vein branches.

• Fig. 25.78 This scan, obtained by scanning transversely in an intercostal space, shows the three hepatic veins. The left hepatic vein has been sampled with duplex Doppler and shows a triphasic wave form which Hepatic artery reflects right atrial and inferior vena caval pressures.

• Fig. 25.79 The right hepatic vein has been sampled in a patient with portal hypertension and ascites due to cirrhosis. This scan shows flattening of the normal triphasic wave form.

• Fig. 25.80 (A) Colorectal cancer metastasis in a patient with a fatty liver following chemotherapy. Note the apparent posterior acoustic enhancement caused by the relative lack of attenuation of the ultrasound beam by the metastasis. (B) Longitudinal scan of the right lobe of the liver and right kidney in a patient with fatty change demonstrating attenuation of the ultrasound beam with the upper pole of the right kidney appearing less reflective than the lower pole. Note the bright liver and loss of vascular detail. (C) Longitudinal ultrasound scan of a patient with an enlarged liver demonstrates an attenuating liver with the beam failing to penetrate posteriorly even using a 2.5 MHz probe. The right kidney appears of relatively low reflectivity. (D) An area of geographical fatty change is seen with a vessel running through this irregular area of increased reflectivity.

• Fig. 25.80 (A) Colorectal cancer metastasis in a patient with a fatty liver following chemotherapy. Note the apparent posterior acoustic enhancement caused by the relative lack of attenuation of the ultrasound beam by the metastasis. (B) Longitudinal scan of the right lobe of the liver and right kidney in a patient with fatty change demonstrating attenuation of the ultrasound beam with the upper pole of the right kidney appearing less reflective than the lower pole. Note the bright liver and loss of vascular detail. (C) Longitudinal ultrasound scan of a patient with an enlarged liver demonstrates an attenuating liver with the beam failing to penetrate posteriorly even using a 2.5 MHz probe. The right kidney appears of relatively low reflectivity. (D) An area of geographical fatty change is seen with a vessel running through this irregular area of increased reflectivity.

• Fig. 25.81 A small area of focal fatty sparing (arrow) in a typical position close to the gallbladder in a patient with an otherwise bright fatty liver which is very attenuating. Note how ill-defined the vessels seem.

• Fig. 25.82 Diffusely echo bright liver in a patient with alcoholic hepatitis and cirrhosis.

• Fig. 25.83 Ultrasound of a cirrhotic liver. There are coarse echoes and vessels are difficult to identify.

• Fig. 25.84 An irregular liver margin with coarse echoes in a patient with hepatitis C cirrhosis.

• Fig. 25.85 Ultrasound using a linear probe demonstrates an irregular liver margin (arrow) in a patient with cirrhosis and no ascites.

• Fig. 25.86 Oblique coronal scan through the porta hepatis of a patient with cirrhosis. Note the irregular liver margin, ascites and coarse liver reflectivity showing normal forward flow (encoded red) within the hepatic artery and reversed flow within the portal vein (encoded blue).

• Fig. 25.87 This scan shows recanalisation of the ligamentum teres with blood flowing in the ligamentum teres toward the Doppler probe, i.e. away from the liver.

• Fig. 25.88 Colour Doppler study demonstrating flow within enlarged collaterals in the position of the coronary vein running along the inferomedial aspect of the left lobe of the liver.

• Fig. 25.89 (A) This scan has been performed without colour Doppler, showing the spleen and left kidney. (B) When colour Doppler is used, abnormal large collateral vessels can be appreciated running between the spleen and left kidney-splenorenal collaterals.

• Fig. 25.90 Colour Doppler study reveals a thickened gallbladder wall containing abnormal vessels with colour flow within them.

• Fig. 25.91 Ultrasound of echogenic bland thrombus partially occluding the portal vein.

• Fig. 25.92 This scan, obtained using an intercostal approach and with colour Doppler, shows a mass of collateral vessels at the porta hepatis, a cavernoma. No normal portal vein can be seen.

• Fig. 25.93 There is tumour thrombus in the portal vein in this patient with multifocal hepatoma in a cirrhotic liver and ascites.

• Fig. 25.94 A transverse intercostal scan. No normal hepatic veins are seen. Some thrombus is seen in a middle hepatic vein. Some abnormal flow away from the probe is seen, with other abnormal collateral vessels close to the surface of the liver with blood flowing out of the liver and coded red.

• Fig. 25.95 (A) Transverse intercostal scan showing the three hepatic veins with colour flow Doppler. Note that because of the poor angle of interrogation of the right hepatic vein, colour flow is not seen within this vessel. (B) In the same position, power flow Doppler has now been used to interrogate the three hepatic veins and flow is readily seen within the right hepatic vein despite the poor angle of interrogation.

• Fig. 25.96 A stent has been placed within a mesocaval shunt and its patency is readily demonstrated with colour flow Doppler.

• shunts. Fig. 25.97 There is a small welldefined lesion with a very thin wall; anechoic contents consistent with a cyst.

• Fig. 25.98 A large intrahepatic cystic mass with calcification within its wall proved to be a biliary cystadenoma.

• Fig. 25.99 Cavernous haemangioma measuring less than 2 cm in diameter demonstrates the typical features of a well-defined hyperreflective mass with some posterior acoustic enhancement.

• Fig. 25.100 There is a heterogeneous mass with some free fluid around the liver. This was subsequently shown to be a large haemangioma which had bled.

• Fig. 25.101 Two lesions in the same patient proved to be due to focal nodular hyperplasia. One deep within liver parenchyma (arrow) is slightly hyper-reflective (A). The other, causing a focal hump on the left lobe of the liver, is of similar reflectivity to normal liver parenchyma (B).

• Fig. 25.102 Ultrasound examination of a patient presenting with right upper quadrant pain and shock due to haemorrhage within an adenoma. Multiple lesions are seen. (A) demonstrates a lesion of similar reflectivity to normal liver with a further area of mixed reflectivity (B). Bleeding had occurred in a superficial lesion (C). The patient later underwent resection of this lesion.

Fig. 25.103 Thick-walled abscess containing mixed reflectivity material with a little through transmission. Enterococcus and Streptococcus species were grown from the pus aspirated under ultrasound guidance.

• Fig. 25.104 An ill-defined area of decreased reflectivy in a pyrexial patient demonstrates some posterior acoustic enhancement (A). The adjacent gallbladder was also abnormal (B). The abscess was successfully drained by inserting a pigtail catheter (arrow) which can be seen within the abscess (C).

• Fig. 25.105 A well-defined area close to the diaphragm containing fine low-level echoes and some posterior acoustic enhancement in a pyrexial patient with a recent history of foreign travel proved to be due to an amoebic abscess.

• Fig. 25.106 The spokewheel appearance of a hydatid cyst.

• Fig. 25.107 A predominantly hyper-reflective mass (arrow) within mass within a cirrhotic liver due to a hepatoma.

• Fig. 25.108 A mixed reflectivity mass within a cirrhotic liver due to a hepatoma.

• Fig. 25.109 A cirrhotic liver with multifocal hepatoma and portal vein tumour thrombus.

• Fig. 25.110 Abnormal colour flow is seen within this focal liver lesion: a hepatoma.

• Fig. 25.111 A hyper-reflective metastasis (arrow) in a patient with carcinoid.

• Fig. 25.112 A larger mixed but predominantly hyperreflective metastasis in a patient with a neuroendocrine pancreatic primary.

• Fig. 25.115 (A) A cystic metastasis with some calcification from ovarian cancer. (B) A small subcapsular (arrow) deposit from ovarian cancer in the same patient.

• Fig. 25.116 A treated metastasis from colorectal cancer exhibiting areas of calcification and an underlying fatty liver.

• Fig. 25.117 (A) Precontrast the liver of this patient with breast cancer has a heterogeneous echotexture. (B) After intravenous contrast (Levovist) with pulse inversion mode there is better definition of metastatic disease. (Courtesy of Shetal Patel.)

• Fig. 25.118 (A) Precontrast a single echogenic breast metastasis may be mistaken for a haemangioma. (B) Postcontrast (Levovist and pulse inversion mode) there is no microbubble uptake in the lesion, confirming the presence of a metastasis rather than a haemangioma.

• Fig. 25.119 A s mall abscess in a patient with hepatic artery thrombosis after liver transplantation. Increased periportal reflectivity is also seen.

• Fig. 25.121 Longitudinal scan of the right lobe of the liver performed shortly after a percutaneous liver biopsy demonstrates a subcapsular collection due to haematoma.

• Fig. 25.122 (A) Longitudinal scan through the liver demonstrating a TIPSS entering the IVC via the hepatic vein. (B) Velocity measurements demonstrate a patent TIPSS with normal flow.

• Fig. 25.123 Ultrasound of the spleen demonstrates a peripheral wedge-shaped area of low reflectivity and lack of power flow consistent with a splenic infarct in a patient with splenomegaly, portal hypertension and left upper quadrant pain.

• Fig. 25.124 Ultrasound of the spleen in a patient with post transplant lymphoproliferative disorder demonstrating diffuse involvement of the tip of the spleen.

• Fig. 25.125 Focal splenic deposits in a patient with chronic lymphocytic leukaemia.

• Fig. 25.126 (A, B) Mixed reflectivity splenic metastases in a patient with ovarian cancer.

• Fig. 25.127 Normal portal vein anatomy. Gd-enhanced T, imaging in RAO projection.

Fig. 25.128 Portal vein thrombosis. Gd-enhanced T, imaging in arterial and venous phases showing normal hepatic arterial supply (A) and replacement of the thrombosed portal vein by varices around the liver hilum (B).

• Fig. 25.129 Portal hypertension. Gd-enhanced T, imaging showing patent portal, splenic and superior mesenteric veins, but large varices along the lesser curve of the stomach (arrows).

• Fig. 25.130 Spontaneous splenorenal shunt. Gd-enhanced T, imaging showing huge varices draining from the hilum of the spleen to the left renal vein in a patient with portal hypertension. S = spleen; LK = left kidney.

• Fig. 25.131 TIPSS. Gd-enhanced T, imaging showing patent portal vein with drop-out of signal along the patent shunt (arrows).

• Fig. 25.132 Budd-Chiari syndrome. Gd-enhanced T, image showing typical feathery pattern of impaired perfusion.

• Fig. 25.133 Liver cysts and cystic tumour. Three small liver cysts show typical appearance of high signal on T 2 (A) and low signal on T 1 images (B). The large cyst appears similar on T2 , but shows high signal on T1, indicating proteinaceous contents or haemorrhage. Gd-enhanced coronal images (C) show enhancing tumour in the wall of the large cyst (arrows). MRCP (D) shows a concurrent hilar tumour obstructing the left and right hepatic ducts

• Fig. 25.133 Liver cysts and cystic tumour. Three small liver cysts show typical appearance of high signal on T 2 (A) and low signal on T 1 images (B). The large cyst appears similar on T2 , but shows high signal on T1, indicating proteinaceous contents or haemorrhage. Gd-enhanced coronal images (C) show enhancing tumour in the wall of the large cyst (arrows). MRCP (D) shows a concurrent hilar tumour obstructing the left and right hepatic ducts

• Fig. 25.134 Hydatid cysts. T2 image shows multiple partially collapsed hydatid cysts in the right lobe producing the 'floating membrane' sign.

• Fig. 25.135 Haemangiomas. Usual appearance of low signal on unenhanced T, (A) and high signal on T 2 (B) with nodular enhancement in the arterial phase (C) and more extensive enhancement in the venous phase (D). The small lesion lying close to the midline (arrow in B) shows typical features; the large right-lobe lesion contains a central core of hyalinised fibrous tissue which remains unenhanced.

• Fig. 25.135 Haemangiomas. Usual appearance of low signal on unenhanced T, (A) and high signal on T 2 (B) with nodular enhancement in the arterial phase (C) and more extensive enhancement in the venous phase (D). The small lesion lying close to the midline (arrow in B) shows typical features; the large right-lobe lesion contains a central core of hyalinised fibrous tissue which remains unenhanced.

• Fig. 25.136 Liver cell adenoma (two cases). T2 images show a heterogeneous mass with predominantly high signal (A); Gd-enhanced T, images (B) show intense but patchy vascularity

• Fig. 25.137 Focal nodular hyperplasia. Unenhanced T, image (A) shows the lesion is slightly hypo intense. Arterial phase Gd-enhanced image (B) shows a central scar with intense parenchymal enhancement, which fades during the venous phase (C), while the central scar shows delayed enhancement.

• Fig. 25.138 Hepatocellular carcinoma. On unenhanced T2 images (A) the rounded mass in the right lobe is slightly hyperintense; after SPIO enhancement (B) the lesion is much more clearly visible. Unenhanced T, image (C) shows a slightly hypo intense lesion; Gd-enhanced images show intense vascularity in the arterial phase (D) with a peripheral capsule appearing on venous phase images (E).

• Fig. 25.138 Hepatocellular carcinoma. On unenhanced T2 images (A) the rounded mass in the right lobe is slightly hyperintense; after SPIO enhancement (B) the lesion is much more clearly visible. Unenhanced T, image (C) shows a slightly hypo intense lesion; Gd-enhanced images show intense vascularity in the arterial phase (D) with a peripheral capsule appearing on venous phase images (E).

• Fig. 25.139 Cirrhosis. SPIO-enhanced T 2 image illustrates the nodular architecture of the cirrhotic liver. Nodules of regenerating liver tissue show SPIO uptake giving low signal, while interstitial bands of fibrosis show relatively high signal.

• Fig. 25.140 Dysplastic nodule. Coronal unenhanced T, image (A) shows a finely nodular liver architecture with a larger nodule of high signal (arrow). Double-contrast technique (B) shows Gd-enhancement in vessels and perivascular fibrosis (high signal) with SPIO enhancement (low signal) in regenerative nodules and the larger dysplastic nodule (arrow).

• Fig. 25.141 Cholangiocarcinoma. MRCP (A) shows obstruction of the left hepatic ducts at the hilum, with less marked dilatation of the right ducts and common duct of normal calibre. Enhanced MIP image (B) shows occlusion of the left main portal vein by tumour. Early (C) and delayed (D) Gd-enhanced T, images show a small tumour at the site of duct obstruction, best seen on the delayed images (arrow).

• Fig. 25.141 Cholangiocarcinoma. MRCP (A) shows obstruction of the left hepatic ducts at the hilum, with less marked dilatation of the right ducts and common duct of normal calibre. Enhanced MIP image (B) shows occlusion of the left main portal vein by tumour. Early (C) and delayed (D) Gd-enhanced T, images show a small tumour at the site of duct obstruction, best seen on the delayed images (arrow).

• Fig. 25.142 Metastases from melanoma. Unenhanced T, image shows multiple lesions with high signal due to melanin content.

• Fig. 25.143 Colorectal metastases. Typical appearance of heterogeneous enhancement on post-Gd T, images (A) and high signal on T2 (B).

• Fig. 25.144 Colorectal metastases. RAO or coronal view is helpful to show the position of metastases relative to the portal vein and IVC. The extensive tumour in this case was successfully resected.

• Fig. 25.145 Hypervascular metastases. Metastases from an islet cell tumour of the pancreas show intense peripheral vascularity in the arterial phase of Gd enhancement (A) which fades rapidly in the venous phase (B). Note that the small lesion arrowed in the arterial phase becomes virtually undetectable in the portal phase of enhancement.