25 DAVID SUTTON FRACTURE THE LIVER AND SPLEEN

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. 25.54 (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. 25.142 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.

25 DAVID SUTTON FRACTURE THE LIVER AND SPLEEN

25 DAVID SUTTON FRACTURE THE LIVER AND SPLEEN

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