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13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
279
Wilson Disease
Copper storage disorder, leads to haemolytic events and early liver insufciency
with relatively unspecic liver changes. Additional neurologic symptoms. US nonspecic in early stage, then increased size and echogenicity; cirrhosis develops in
later stages.
α1-Antitrypsin Deficiency
Most common cause of “hepatitis syndrome” in infancy. US in early phases nonspecic, potentially some enlargement+homogenous alteration of texture similar
to hepatitis. Course/severity varies, eventually may lead to liver cirrhosis
(Fig.13.9a).
Haemosiderosis
Iron deposit in liver—either idiopathic or secondary to various systemic/haemolytic
conditions. US nonspecic: enlargement, in early phase, smooth surface and
rounded lower margin with increased echogenicity. Over time more nodular parenchymal aspect develops. The further course depends on severity and management of
underlying condition.
Note Specic MR techniques and programmes using susceptibility phenomena on
T2-star-weighted sequences allow (semi-)quantitative assessment of iron content—
reliable monitoring during therapy and follow-up.
Role ofUS
Most commonly used imaging modality for diagnosis and follow-up of liver
conditions.
• Particularly CDS, ce-US and complementary dynamic sectional imaging (most
commonly MRI) can be helpful—particularly for focal disease.
• Increasingly US elastography also applied to children with liver disease: elevated
maximum shear wave velocities and high stiffness (e.g. above 18.8—2m/s, but
normal values depend on transducer and device) seem to be indicative for brotic/
cirrhotic changes.
• Depending on query (M)ERCP may be indicated in conditions affecting the bili-
ary system.
13.3.4.4 Portal Hypertension andVascular Problems
Portal Hypertension
Definition
Increasing liver resistance with increase of PV pressure above 10 mmHg. Most
common and important vascular liver disease. Pressure measurement not feasible
by US, but indirect signs on grey scale and CDS/spectral analysis enable reliable
assessment in diagnosis and follow-up of suspected portal hypertension. Details of
underlying conditions are in their respective sections.
280
M. Riccabona
Causes typically placed into three broad categories:
• Prehepatic: portal vein obstruction/occlusion/thrombosis/stenosis.
• Intrahepatic/intra-sinusoidal: parenchymal disease with increased resistance of
the peripheral sinusoid vascular bed (some also place peripheral intrahepatic PV
impairment in this group).
• Posthepatic: HV problems, increased intrathoracic/right atrial pressure.
US Criteria
Findings of underlying condition (e.g. liver brosis/cirrhosis, hepatomegaly, periportal brosis).
• Commonly hilar PV tapering: enlargement of prehepatic portion, narrower intra-
hepatic portion, except for prehepatic origin.
• Secondary splenomegaly with tortuous vessels at splenic hilus.
• Portosystemic anastomoses: splenorenal, splenogastric, from spleen to abdomi-
nal and thoracic wall to diaphragmatic vessels/gastric veins with secondary
oesophageal varices, recanalisation of umbilical vein, collateral vessels from
liver hilus to gastric veins, etc. Secondary dilatation of draining venous vascular
system with formation of anastomotic venous networks (abdominal wall around
the umbilicus—“caput medusa”, inferior mesenteric anastomoses to rectoanal
veins with haemorrhoids, tubular enlarged mesenteric veins with congestive
changes of mesentery and bowel wall), secondary ascites.
• PV thrombosis may be primary and causative or secondary to reduced portal ow.
• Secondary cavernous transformation with development of veins in PV wall (mul-
tiple tubular tortuous small lumen veins at liver hilus without visualisation of
normal PV).Flow usually insufcient to prevent portal hypertension. May recon-
stitute normal appearing intrahepatic PV.
Doppler Criteria
• HV: veins difcult to nd (CDS helpful), reduced undulation—potentially band-
like ow spectrum. Often reduced ow, slow velocity.
• PV: initially increased undulation, then loss of undulation of PV ow. Reduced ow
velocities, eventually bidirectional or hepatofugal inverted ow direction (Fig.13.10).
• HA: secondary to reduced PV ow, arterial liver perfusion increases. HA
becomes larger, very pulsatile, with high (particularly systolic) velocities.
US Depiction of Portal Systemic Shunts
• CDS may directly visualise abnormal venous pathways (e.g. recanalised umbili-
cal vein, varices at gastrooesophageal junction, splenorenal shunts, inverted ow
in superior mesenteric vein).
• If no collaterals are seen, ow volume measurements of PV, splenic+superior
mesenteric vein may be helpful (indirect sign): PV-volume ow should be equal
or higher than sum of volume ow of splenic vein+superior mesenteric vein—
otherwise there must be some shunt somewhere.
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
Fig. 13.10 Portal hypertension: (a) Inverted hepatofugal ow in central portal vein encoded in
blue (next to red encoded HA) due to portal hypertension with intrahepatic block. (b) Duplex ow
analysis conrms the inverted direction of portal venous ow. (c) CDS demonstrates lack of ow
in central portal vein due to extrahepatic portal vein thrombosis in a patient after liver
transplantation
281
Note These measurements are cumbersome in small children, heavily rely on good
angle correction at reasonable Doppler angles as well as accurate cross-sectional
assessment of vessel diameter. Due to underlying equation even mild errors in vessel area/diameter measurements cause enormous changes in calculated volume ow
(see chapter on Doppler US).
In portal vein thrombosis/prehepatic block: lack of visualisation of PV ow
(Fig.13.10c)—recanalisation or cavernous transformation can also be assessed.
Note Thrombi can reach into splenic or superior mesenteric vein—these vessels
always need to be assessed for patency or involvement.
Vascular Malformations
Intrahepatic vascular malformations or other pathology are rare, but many normal
variants, particularly of origin and number of hepatic arteries.
May be idiopathic/congenital, secondary after trauma/surgery/transplantation,
in/after inammation (e.g. mycotic or inammatory aneurysm), or connected with
systemic vascular disease (Kawasaki, ADPKD Type I, bromuscular dysplasia, etc.).
• Arteriovenous/arterioportal shunts/stula: vary in size, (multi)focal or even dif-
fusely generalised; depictable as cyst-like lesion on grey scale, eventually identi-
ed as such by CDS.
• Postoperative or posttraumatic stula: usually only depicted on CDS, shunt ow
assessed by spectral analysis of feeding and draining vessel(s).
• Aneurysms: ectatic cyst-like vessel changes—use CDS, turbulent ow, alternat-
ing bidirectional ow jet, may (partially) thrombose (Fig.13.11c, d).
• Vessel malformations such as aberrant drainage of pulmonary veins (e.g. Scimitar
syndrome) or combined with cardiac malformations—ow vessels from origin
to drainage point.
282
Fig. 13.11 Posttraumatic AVF in liver, other vascular liver malformations: (a) CDS reveals high-
velocity turbulent ow in a posttraumatic arteriovenous stula. (b) Duplex trace analysis conrms low
resistance arterial ow in the feeding artery and arterialised ow in draining vein. (c) Portal vein aneu-
rysm after liver transplantation at site of anastomosis. (d) CDS reveals turbulent ow in the aneurysm
M. Riccabona
• Haemangioma/haemoendothelioma etc.: vascular malformations—see below
under liver tumours.
US and CDS Findings
Depend on entity and size (Fig.13.11).
In shunts, CDS may enable depiction of arteriovenous stula and visualise
hyperperfusion of feeding vessel with secondary arterialisation of draining vein
(PV, HV) (Fig.13.11a, b). PV shunts rare and difcult to nd.
Portal Vein andHepatic Artery Stenosis
Extremely rare in childhood, same conditions and features/criteria as in other vessels apply. More common after transplantation or surgery.
US and CDS Findings
• Change in diameter.
• Regional ow turbulence with aliasing.
• Pre- and poststenotic ow pattern alteration with delayed systolic upstroke, long
acceleration time (pulsus tardus et parvus).
• Turbulent diastolic ow.
• Turbulence and increased velocity at site of stenosis, etc.
Note All ndings depend on severity and grade of stenosis.
Congenital Agenesis or Variants ofPortal Vein/Congenital Portocaval
Anastomosis/Abernethy Malformations
Variety of conditions, extremely rare—lead to liver failure/brosis.
US and CDS Findings
• Non-visualisation of portal vein (Fig.13.12).
– Anomalous vessels connecting splanchnic veins to central circulation.
– Resultant arterial hyperperfusion to compensate for lack of PV perfusion.
– Often develop FNH and/or adenomas, may have malignant course.
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
Fig. 13.12 Abernethy malformation: (a) Huge nodular liver structural alteration (++) in a 9-year-
old girl with Abernethy malformation—likely to present an FNH. (b) CDS of liver hilus vessels
demonstrates lack of a normal portal vein entering the liver. The splenic and mesenteric veins drain
into an unusual venous connection to the inferior vena cava (coded in blue). The more orange
coded vessel is the reactively enlarged hepatic artery
283
Hepatic Vein Thrombosis/Occlusion/Stenosis
Summarises variety of conditions, most typical ones:
Budd–Chiari Syndrome
Large veins obstructed/occluded by space-occupying lesion compressing the vessel
or by thrombosis.
Veno-Occlusive Disease (VOD)
New name=Sinusoidal obstruction syndrome: affects small peripheral portions—
obstruction and thrombosis/brosis of small sinusoidal venules after necrosis of
hepatocytes due to sinusoidal injury/disease. Typically a complication after chemotherapy or radiation for bone marrow transplantation, particularly after Wilms’
tumour. Peripheral disease, thus only depictable by indirect US signs.
Increased Right Atrial/Intrathoracic Pressure.
Secondary to cardiothoracic conditions.
Note The loss of typical HV ow modulation is very sensitive for veno-occlusive
disease, but not specic. Any other cause that either increases hepatic resistance and
stiffness or elevates right atrial pressure will cause similar phenomena. However,
HV spectral analysis helpful for follow-up to document improvement and recovery
by demonstrating increasingly normal ow patterns during treatment.
Portosystemic Shunts
Secondary to portal hypertension or vascular malformation/anomaly (see above).
Surgically introduced shunts—for treatment of portal hypertension, including TIPS.
CDS used to assess patency of shunts; spectral analysis after proper angle correction allows quantication; helpful for follow-up and reveals complications such as
occlusion, thrombosis or stenosis.
284
M. Riccabona
Persistent ductus venosus also causes shunting between the left PV and systemic
venous circulation.
• Shunt direction and ow velocity can be measured (see Fig.13.2a, b). A persist-
ing venous duct is usually sign for underlying liver disease and rarely a vascular
problem itself.
13.3.4.5 Liver Trauma
Liver laceration or contusion is relatively common in paediatric blunt abdominal
trauma. However, early after trauma, even severe injuries are easily missed by US
due to similar echogenicity of fresh blood and liver parenchyma—follow-up after
12–24h is essential, or the use of UCA.
Therapy and prognosis as well as risk of complications depend on grade, thus
also US should try to establish a grading (Table13.4).
US after intravenous UCA administration signicantly improves US potential to
diagnose injuries early, with similar sensitivity as CT and may even visualise active
bleeding (BUT: at present UCA in paediatrics off-label).
Table 13.4 Liver injury
grading system
Grade I
Haematoma: Subcapsular, <10% surface area
Laceration: Capsular tear, <1cm depth
Grade II
Haematoma: Subcapsular, 10–50% surface area
Haematoma: Intraparenchymal, <10cm diameter
Laceration: Capsular tear, 1–3cm depth, <10cm length
Grade III
Haematoma: Subcapsular, >50% surface area or
ruptured with active bleeding
Haematoma: Intraparenchymal, >10cm diameter
Laceration: Capsular tear, >3cm depth
Grade IV
Haematoma: Ruptured intraparenchymal with active
bleeding
Laceration: Parenchymal disruption involving 25–75%
hepatic lobes or
1–3 Couinaud segments (within one lobe)
Grade V
Laceration: Parenchymal disruption involving >75%
hepatic lobe
>3 Couinaud segments (within one lobe)
Vascular: Juxtahepatic venous injuries (IVC, major
hepatic vein)
Grade VI
Vascular, hepatic avulsion
Adapted from American Association for Surgery of Trauma
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
285
Liver Haematoma
Simple haematoma or subcapsular haemorrhage is usually less threatening, may
become more serious if liver capsule is ruptured and signicant free peritoneal uid
seen (potentially with more or less sedimentation depending on time of
investigation).
Note Free peritoneal uid/blood appearing like complicated ascites can be found
anywhere in abdomen and does not necessarily correlate with site of injury, as uid
redistributes depending on positioning and other phenomena.
US Findings
Initially same echogenicity as liver parenchyma, potentially disruption of other
structures such as vessels or outer contour can aid diagnosis (Fig.13.13a). Thereafter
appear hyperechoic, eventually turns hypoechoic with more or less complex appearance. Persisting hypoechoic posttraumatic lesions indicate seroma/cyst or even
biloma (the latter particularly when growing) (Fig.13.13d).
• CEUS can be helpful in equivocal situations.
Contusion
More difcult to diagnose, often triangular in shape, located in subcapsular.
a
b
c
de
Fig. 13.13 Liver trauma: (a) Large subcapsular liver haematoma (++), reactive ascites and pleu-
ral effusion. (b) Liver laceration—initial baseline US scan. (c) ce-US (CEUS) (same patient as in
b) clearly delineates the liver laceration in early phase. (d) Cystic transformation of old liver haematoma (seroma—difcult to differentiate from biloma). (e) CEUS for liver trauma using a dual
image (left side grey scale mode, right contrast mode): grey scale rather poorly shows the huge
defect (left image) nicely outlined by CEUS (right image)
286
M. Riccabona
US and CDS Findings
Initially difcult to see, echogenicity changes from hyperechoic to hypoechoic.
(a)CDS may improve detection of contusions by focal disruption of normal vas-
cular architecture with regional rarefaction of vessel colour signals.
Laceration
Definition
Disruption of liver parenchyma and capsule.
US Findings
Discontinuity of contour may be primary nding—despicable even in early stages.
• ce-US (CEUS) will aid early diagnosis (Fig. 13.13b, c, e). Often appears
hypoechoic, whereas surrounding tissue inhomogenously patchy, with more or
less echogenic areas. Local haematoma will coexist (see above).
Note Pay particular attention to involvement of major structures such as major bile
ducts, central PV or involvement of HVs (may develop occlusion and thrombosis
causing necrosis of respective liver segment). If extrahepatic hypoechoic collections
persist after liver trauma, consider bile leakage and biloma.
Haemobilia
Haemorrhage into bile ducts—sludge-like echoes in bile ducts/gall bladder.
Associated Diaphragmatic Injury
Rarely diaphragm can be involved. Detectable commonly just by reactive palsy with
high position of upper liver border+subphrenic haematoma+reactive pleural effusion (common).
If diaphragm ruptured, US may be able to demonstrate herniation of liver or
haematoma into thorax.
Reliable assessment of integrity and continuity of entire diaphragm is impos-
Note
sible by US, particularly on left side.
Liver Infarction
Rare traumatic nding due to dual blood supply, more common after transplantation
or surgery and more common in HA than PV, usually branch occlusion. Potentially
also more diffuse after severe shock with diffuse hypoperfusion and hypooxygenation of liver. Other rare causes are systemic vascular or haemolytic disease.
US and CDS Findings
• Typically wedge shaped, round to oval hypoechoic area with indistinct margins
and peripheral distribution reaching to subcapsular area. Secondary necrosis
with cystic structures or even hyperechoic foci representing gas, secondary calcication and bile lakes. CDS—lack of perfusion in affected vessel.
• CEUS may be helpful.
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
287
Role ofUS inLiver Trauma
First imaging modality in moderate blunt abdominal trauma—need to perform more
than just FAST (“focused abdominal US for trauma”, as performed in emergency
room for detection of free uid). Detailed study in any stable patient can help to
reduce need for (or for tailoring) CT.US follow-up after 6–24h is essential. CEUS
improves lesion detection, particularly in early phase (see Fig.13.13).
Note Ce-CT is mandatory (after FAST) in severe and multiple trauma—US may
additionally miss signicant injuries of retroperitoneal structures, bowel and spine,
as well as chest involvement; US ndings may serve as indicator injury.
Additional Imaging
• Acute setting/severe and multiple trauma: Ce-trauma-CT mandatory.
• For assessing equivocal lesions in stable patient/follow-up: dynamic ce-CT increasingly replaced by ce-MR for radiation protection; consider CEUS if available.
• Abdominal plain lm—no utility.
• Chest lm—usually performed in multiple trauma in ER.
13.3.4.6 Space-Occupying Liver Lesions
Simple Cysts
Commonly congenital, usually an incidental nding, rarely asymptomatic.
Other causes: posttraumatic, after (displaced) umbilical vein catheter, after
abscess, after surgery, bile leakage and biloma, infectious, biliary malformations/
cysts, cystic/necrotic part of tumour.
US Findings
Anechoic uid, spherical, thin and smooth wall, no parenchymal nodules
(Fig.13.14).
Note As soon as there are septae, parenchymal areas or thick wall-like membranes,
other entities such as abscesses, hydatid cyst, epidermoid cyst (potentially with
complex content) must be considered (see Fig.13.15).
Fig. 13.14 Cystic liver lesions. Huge,
but otherwise simple liver cyst
288
bc
a
M. Riccabona
d
Fig. 13.15 Complicated liver cysts: (a) Complicated liver cyst with sedimentation—probably post-
traumatic. (b) Complicated liver cyst after a liver abscess. (c) Complicated liver cyst with split wall
and septations—a hydatid cyst. (d) Complex cystiform lesion (++) after surgery that proved to be a
biloma. (e) Large polycystic liver haematoma imaged using panoramic imaging—on imaging sometimes indistinguishable from any other complicated “cystic” mass—with corresponding ce-CT image
e
Complicated Cysts
Different causes, postinfectious/posttraumatic/postsurgical or hematogenous/
ascending inammatory disease and cystic tumours.
US and CDS Findings
Similar to simple cysts, but additionally oating echoes, septae, thick wall or parenchymal nodules (Fig. 13.15). Need at least follow-up or additional diagnostic
efforts. Sometimes resected/punctured, particularly in suspicion of tumour or for
(sclerosing) therapy.
CDS may nd vascularisation of wall, septae or parenchymal nodules.
Liver Calcifications
Variety of causes such as after haemorrhage, abscess, bile duct concretion, cholangitis, Caroli syndrome, cystic brosis, inammatory (viral, particularly foetal infections) and meconium peritonitis (capsular calcications). US usually cannot dene
aetiology.
US and CDS Findings
• Echogenic spots of varying size with dorsal shadowing, depending on amount of
calcium/size (Fig.13.16).