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7.1 Requisites and Investigation
215
sometimes assessing deeper compartments or subdiaphragmatic areas, sector array
helpful.
Linear transducers recommended for assessing liver surface and details of parenchymal structure as well as common bile duct and gall bladder wall
High-resolution linear arrays (potentially using trapezoid format) recommended
in neonates and infants.
Frequency range depends on age and size (2–15 MHz).
Harmonic imaging, image compounding, speckle reduction and other sophisticated post-processing options helpful. Thorough study always includes colour and
spectral Doppler analysis; aCDS less useful in liver.
NOTE : For improving lesion detection and characterisation, IV ce-US particularly
helpful – although currently no US-CM registered for paediatric use.
7.1.4 Course of Investigation
Liver usually assessed from ventral and lateral, rarely dorsal approach necessary or
helpful. Systematically sweep through entire liver in sagital, axial and oblique sections. follow course of major structures (portal nvein liver veins), assess gall bladder, and eventually add Doppler if indicated.
Small children do not respond to positioning commands – use respiration or ask
them to “take deep breath” may enable assessment, particularly of subdiaphragmatic areas.
7.1.5 Standard Planes
• Sagittal section in sternal line (STL), left and right in middle clavicular line
(MCL) and right ventral, middle and posterior axillary line (V/M/PAL)
• Axial sections particularly focused on portal vein and hilar structures – from
ventral and lateral approach
• Oblique sections tilted cranially for meticulously scanning entire liver, particu-
larly for documentation of portal vein branching, hepatic veins and gall
bladder
• Standardised documentation (VAL – defi ned by upper pole of right kidney, MCL
– commonly defi ned by gall bladder, STL – defi ned by abdominal aorta), section
through hepatic veins, portal vein branching, main portal vein (if not included
gall bladder view) (Fig. 7.1 ) ( www.oegum.at )
NOTE : Due to complexity of the liver, documentation and measurements in
standardised sections are essential. For identifi cation of section – include other
key structures on image, particularly important for comparison during
follow-up.
216
a
7 Liver and Bile System
b
Fig. 7.1 Standard liver measurements and liver segments: ( a ) Liver anatomy with liver segments
( I – VIII ), relevant liver vessels for anatomical classifi cation (portal vein, hepatic vein, inferior vena
cava) and standard planes for US measurements, particularly right anterior axillar line ( AL ), right
and left middle clavicular line ( r / lMCL ) and medially positioned sterna line ( STL ). Two respective
normal sagittal views with important reference structure (upper pole of right kidney for AL,
abdominal aorta for STL) given. ( b ) Standard image appearance of typical liver sections: the trans-
ducer position and orientation given in the schematic drawing, with respective US images
7.2 Normal Findings
7.2.1 Structure
Liver has larger right and smaller left lobe, internal architecture classifi ed by liver
segments (Fig. 7.1 ).
Parenchyma – homogenous echo of medium echogenicity, contour and borders
as well as sharp and smooth margins. Size varies with age, particularly height –
measurements correlated with normograms (Table 7.1 ).
NOTE : Physiologically left liver lobe is much larger in neonates than in older ages;
it gradually shows relative decrease in size after closure of ductus venosus.
7.2 Normal Findings
217
7.2.2 Ligaments
Ligamentum falciforme hepatis, ligamentum teres hepatis and ligamentum triangulare hepatis fi x liver within abdomen, usually only seen with ascites.
7.2.3 Hepatic Veins (HV)
Converge cranially to drain into subdiaphragmatic inferior cava vein (ICV) or into
right atrium. usually three main liver veins (+ caudate vein); additional veins or
varied insertion at different levels of intrahepatic ICV exist as normal variants. Size
may vary with respiration and intravascular volume – usually exhibit smooth border
and straight course, with relatively thin low echogenicity wall.
7.2.4 Portal Vein (PV)
Enters at hepatic hilus, should not show tapering (a sign of portal hypertension).
Branches between left and right PV in liver centrally, left PV shows focal ectasia
(Rex recessus, sinus venosus) at area of former insertion of umbilical vein draining
via venous duct of Arantii (ductus venosus) to right atrium during fetal circulation.
Wall slightly more echogenic, partially increased by periportal structures (bile
ducts, accompanying arteries). Periportal region gets enlarged and more echogenic
in various conditions or may appear prominent with decreased echogenicity of liver
parenchyma.
NOTE : In neonates (during fi rst weeks of life), communication may persist between
sinus venous and ICV/right atrium (“physiologically persistent ductus venous”
Fig. 7.2a ) – should obliterate spontaneously. Persistent ductus venosus usually indi-
cates underlying liver disease with increased peripheral liver resistance. Umbilical
Table 7.1 Normal liver size in relation to age/height
Measurements of body height related (cm) normal liver size (cm) during childhood
218
ab
Fig. 7.2 Neonatal liver: ( a ) Physiologic persistent ductus venosus (+ +). ( b ) Flow and patency of
neonatally persistent ductus venosus depicted by CDS – fl ow direction documented by Doppler
trace. ( c ) Still visible umbilical vein with catheter ( arrow )
7 Liver and Bile System
c
vein may be visible in neonates physiologically, but shows no fl ow – consequently
thromboses and vanishes; persisting (inverted) fl ow in umbilical vein – sign for
portal hypertension and consequent portosystemic shunt. A nonfunctioning umbilical vein catheter may end in this vein – actively search for it (Fig. 7.2b ).
7.2.5 Hepatic Artery (HA)
Can be followed from its origin at coeliac trunk parallel to PV to branching into left
and right HA.
Usually CDS enables easy identifi cation and differentiation from other tubular
structures, particularly in liver periphery, where differentiation of HA from (dilated)
intrahepatic bile ducts is otherwise diffi cult.
NOTE : Numerous normal variants in HA anatomy, e.g. accessory left HA from
coeliac trunk or gastric artery, separate origin of right HA from superior mesenteric
artery. CDS particularly valuable for assessing these anatomic variants.
7.2.6 Gall Bladder
Positioned on lower surface of liver, centrally close to hilus on right side. Usually
shows thin wall, contents unechoic. Size can vary with time since feeding. Best seen
in subcostal oblique view in MCL.
NOTE : An empty or poorly fi lled gall bladder, particularly if relatively large when
fi lled, may show a pseudothickened wall (Fig. 7.3a ).
7.2.7 Common Bile Duct (Commonly Addressed
as Hepato- Choledochal Duct)
Usually crosses main PV and runs through head of pancreas to papilla/ampulla of
Vater.
7.2 Normal Findings
a
219
bc
Fig. 7.3 Bile system: ( a ) Normal, nearly empty gallbladder (+.....+) with pseudothickening of
wall. ( b ) Normal common hepatic duct (
tion shows pancreatic portion of prominent common bile duct
3, 2
+ +), confl uence with cystic duct ( 1 + +). ( c ) Axial sec-
NOTE : Duct (even ductus cysticus) often visible using high-resolution linear trans-
ducers (Fig. 7.3b, c ).
7.2.8 Intrahepatic Bile Ducts
Course parallel to PVs – usually only depicted centrally or if dilated.
7.2.9 Doppler Findings
7.2.9.1 Hepatic Veins (HV)
Show bi- or triphasic undulating fl ow pattern, bidirectional fl ow direction.
Undulation caused by respiration and heart cycle (Fig. 7.4a ). Absence of typical
pattern usually indicates either increased liver resistance or increased right atrial
pressure/volume overload.
NOTE : Flow profi les may vary within the three main veins, also depends on point of
insertion and manoeuvres used for visualisation (such as breath holding). Undulation
must always persist; bidirectional or triphasic pattern may physiologically be absent.
7.2.9.2 Portal Vein (PV)
Usually shows constant fl ow into liver with some mild respiratory modulation
(Fig. 7.4b–d ).
Flow velocities vary with age (Table 7.2a ) and fasting status.
NOTE : Also intrahepatic PV branches should be assessed to show patency of at
least main right and main left PV. Flow velocity measurements strongly rely on
proper angle correction and good insonation angle (<60°).
7.2.9.3 Hepatic Artery (HA)
• Less often important
• Systolic velocity varies with age and nutritional status (Table 7.2b ), as does dia-
stolic velocity/RI
220
a
bc
7 Liver and Bile System
d
Fig. 7.4 Liver vessels: ( a ) Hepatic veins, bidirectional undulating fl ow demonstrated by CDS
(either red or blue signals indicating two fl ow directions during respiratory cycle) with cardiac and
respiratory modulation also demonstrated by spectral fl ow analysis. ( b ) Main portal vein entering
liver: note no signifi cant variation in diameter. ( c ) Portal vein fl ow on CDS ( red colour signals ):
note adjacent hepatic artery with faster fl ow in same direction (coded in orange ). ( d ) Duplex-
Doppler fl ow profi le confi rms normal hepatopetal portal fl ow +1 indicates maximum velocity
• CDS essential for differentiating particularly peripheral branches from biliary
structures and for proper angle correction (if fl ow velocity measurements taken).
NOTE : HA shows same fl ow direction as portal vein – only by selecting proper
CDS settings (gate, fi lter, fl ow velocity) – discrimination of PV and HA feasible on
CDS.
7.2.10 Special Aspects of Newborns and Infants
• After closure of ductus venosus – relative increase in size of the right liver lobe
– neonates have signifi cantly larger left liver lobe than older children. Left and
right liver lobes may even be similar in size
• Newborns’ liver softer and more fl exible – slightly rounded lower margin is
physiologic
• Parenchyma less differentiated and less echogenic than in older age due to
reduced fi brosis and less fat – compared to renal cortex liver parenchyma echo-
genicity is lower
7.2 Normal Findings
Table 7.2 Normal values for liver vessel fl ow
(a) Normal fl ow in portal vein
Rule of thumb : above 20 cm/s in non-fasting child (general lower cut-off value):
With some respiratory undulation
Flow pattern and – to a lesser degree – fl ow velocities infl uenced by respiration:
More undulating fl ow in earlier years than later in childhood.
In healthy term neonates peak portal blood fl ow may double 15 min after feeding:
Fasted = 24 ± 1.3 cm/s after feeding = 35.9 ± 2.4 cm/s
(b) Age-dependent fl ow velocities in hepatic artery
Age
( years )
diameter
( mm )
0–5 3.5 ± 2 9.1 ± 70 ?
6–12 6.3 ± 2 13.4± 250 ? (50–100)
PV
PV
velocity
( cm/s ) PV fl ow ( ml/min )
HA
velocity
( cm/s )
a
? (85 ± 15) a
HA RI
( % )
a
? (60 ± 10) a
>12 7 ± 2.6 14.6 ± 5 380 70–120 60 ± 4
Average values are not applicable, as velocities are very low in neonates (around 40 cm/s),
even lower in preterm babies, and increase relatively quickly to values similar to older
children – HA hepatic artery, PV portal vein
a
No established normal values – the numbers given for orientation are from individual reports
and own experience, particularly in neonates
(c) Hepatic vein fl ow profi le
221
Schematic drawing of typical fl ow patterns of hepatic veins (Types I–IV), and how elasticity
index (EI) is calculated (EI = a/b %)
(d) typical fl ow patterns of heaptic veins
Type I Normal Triphasic, bidirectional
EI ~ 120 %
fl ow
Type II Unspecifi c Triphasic, monodirec-
EI ~ 90 %
tional fl ow
Type III Dampened Tonodirectional, but
EI ~ 40 %
still modulated fl ow
Typ IV Severely
impaired
Monodirectional,
uniform, unmodulated
EI ~ 0 %
fl ow
222
• Periportal echoes less prominent
• Ductus venosus can remain patent up to some weeks – seen as tubular vascular
structure coursing from ectatic section of left PV to ICV/right atrium. Closes
spontaneously – then seen as echogenic band (= ligamentum venosum in later
age) (see Fig. 7.2a, b )
• Unusual or altered fl ow patterns in neonates do not always indicate hepatic disease; often refl ect physiologic systemic or vascular variations (e.g. patent foramen ovale, PDA, persistent ductus venosus Arantii). Interpretation of Doppler
fi ndings needs to be made with care and respect to all other clinical and laboratory data as well as imaging fi ndings; sometimes additional assessment of
abdominal aorta, renal or cerebral vessels, heart and other large vessels necessary for deciding on origin of unusual fl ow fi ndings
7 Liver and Bile System
7.3 Pathology of the Liver
7.3.1 Congenital Changes and Normal Variance
7.3.1.1 Situs Inversus (Abdominalis)
Defi nition
Liver on left side, no isolated liver malformation.
US Findings
Liver seen in left upper quadrant, spleen situated in right upper abdomen (potentially
with multiple splenunculi – polysplenia syndrome). Liver anatomy is mirrored.
7.3.1.2 Butterfly or Midline Liver
Defi nition
Often associated with other (systemic) malformations and syndromes (e.g. ambiguous situs, polysplenia syndrome, asplenia, gastroschisis and omphalocele).
US Findings
Butterfl y-shaped liver positioned medially, often hilus structures in unusual position
and relation, more diffi cult to fi nd and identify. Left and right liver lobes often of
similar size. HVs drain directly into right atrium or into hemiazygos continuation of
interrupted ICV.
7.3.1.3 Hypoplasia/Atrophy of Left Liver Lobe and Other Variations
Hypoplasia is usually a consequence of intrauterine events – not congenital or
hereditary, only conatal malformation.
Other variants are diaphragmatic bump fi lled with liver, variations associated
with diaphragmatic hernia and liver up-position, variations associated with gastroschisis and omphaloceles.
Many variations both of arterial and venous anatomy are most identifi ed by
proper technique using CDS. Have little other implication – unless liver surgery or
transplantation planned.
7.3 Pathology of the Liver
223
7.3.2 Inflammatory Conditions
7.3.2.1 Hepatitis
Defi nition
Mostly viral in origin. May occur in any time of childhood, even neonatally. Shows
large variance in its course and outcome.
During its course there may be fi brosis, other diffuse hepatopathies, enlargement
or shrinkage, eventually cirrhosis or secondary abscess formations.
US Findings
Unspecifi c – liver normal or slightly enlarged. Usually surface remains smooth,
lower margin slightly rounded. Echogenicity more or less decreased, with normal
appearance of periportal area, unless signifi cant decrease in parenchymal echogenicity – then periportal regions become prominent. Associated oedematous
changes of gall bladder wall and bed possible (DDx: cholecystitis, congestive, vasculitis such as Kawasaki disease, during intensive care).
Associated fi ndings: enlarged lymph nodes in hepato-duodenal ligament,
splenomegaly.
CDS
Hyperaemia with low RI of HA, potentially increased PV fl ow; in severe enlargement and thus increase in liver resistance also reduced undulation in HV.
NOTE : US does not allow defi nition of aetiology or discrimination between viral,
bacterial, toxic, drug-induced or other forms of hepatitis/hepatopathies. Mimics exist.
7.3.2.2 Liver Abscess
Defi nition
Usually haematogenous, sometimes ascending through bile ducts.
Various entities – bacterial, fungus, secondary after malignant infi ltration, echinococcal or other parasites (amoebiasis, ascariasis, schistosomiasis, etc.).
US Findings
Spherical or polygonal focal alteration of liver texture. If necrotic – central
hypoechoic, sometimes with (fl oating) echoes, in complex abscess formations
increased central echogenicity, fl uid levels. Usually peripheral membrane and halolike peripheral hypoechogenicity (Fig. 7.5 ).
Image varies with course – only subtle fi ndings in beginning, more pronounced
in later stage.
Other focal liver lesions sometimes diffi cult to differentiate (metastasis and infi l-
tration in systemic haematologic disease).
CDS
Shows central avascular nature with peripheral membrane-like hypervascularisation
and hyperaemia. Reactive diffuse hyperaemia of HA and PV.
If associated with ascending condition, gas or air bubbles seen in peripheral bile
ducts – causing small echoes with reverberation and twinkling on CDS (aerobilia).
Spectral trace shows blip-like short high-amplitude partially bidirectional signals.
224
7 Liver and Bile System
ab
Fig. 7.5 Liver abscess. ( a ) Focal nodular hypoechoic disruption of liver parenchyma and several
initial small lesions – in this case fungal septicaemia in oncology patient during chemotherapy
(fungal abscess). ( b ) CDS may confi rm the necrotic avascular nature and show peripheral, mem-
brane-like hypervascularisation
Table 7.3 Hydatid disease – grading system (Gharbi classifi cation)
Type I: pure simple cystic fl uid collection
Type II: cystiform fl uid collection with split, nodular-irregular wall; may contain echoes in
central compartment
Type III: cyst with complex fl uid collection and internal septae
Type IV: cyst with heterogenous echo pattern, potentially beginning calcifi cations
Type V: cyst with refl ecting thick walls (mature/old form), often has calcifi ed walls
ab
Fig. 7.6 Echinococcus: ( a ) Two hydatid cysts with complex inhomogenous content (stages 3–4).
( b ) Extended view delineates huge hydatid cyst with slightly complex fl uid and septations in left
liver lobe (stage 3)
Special Entities :
• Echinococcal/hydatid disease: manifest as cystic liver lesions; different appearances depending on age and stage (Type I –Type IV, Gharbi classifi cation used
most commonly) (Table 7.3 ) (Fig. 7.6 ). In children Type I and III commonly
seen (younger manifestation). Differentiation of Type I lesion from other
hepatic cysts diffi cult. US used for puncture and therapeutic alcohol/drug
instillation