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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5795_Библиотеки_им_академика_М_И_Перельмана.pdf
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
299
• Within cysts there may be sludge and sedimentation—due to cholestasis, secondary infection, haemorrhage, etc.
• Often underlying/associated condition—“common channel” of pancreatic and
choledochal duct before entering sphincter mechanism, usually not depictable by US.
• Secondary changes depend on severity and duration/time of diagnosis, may
range from normal liver appearance to liver brosis or biliary cirrhosis.
• Long list of DDx, particularly in neonatal hyperbilirubinemia/jaundice (see
Table13.5).
Complications
• Large cysts can rupture—cause biliary peritonitis.
• Choledochoceles may protrude into duodenum.
• Associated recurrent pancreatitis—may cause changes in echogenicity and size
of pancreas+prominent margin of slightly irregular pancreatic duct.
• Stone formation.
• Thickened wall of (enlarged) gall bladder with secondary cholecystitis.
• Ascending cholangitis.
• Intrahepatic abscess.
• Neoplastic transformation—most commonly adenocarcinoma.
Note In Caroli disease both types are possible and associated with cystic renal disease (ciliary complex)—saccular dilatation+brotic type with portal hypertension.
13.4.3 Biliary Tract Diseases
13.4.3.1 Aerobilia
Definition
Air in intrahepatic bile ducts (postoperative, ileus, obstruction, etc.).
US and CDS Findings
• Echogenic material with reverberation artefacts in periportal eld.
• Differentiation from portal venous air may be difcult.
• DDx to portal venous gas: No gas bubbles depictable in central portal vein
(duplex-Doppler trace—see above, Fig.13.17).
• CDS: Twinkling sign—similar to calcications/intrahepatic bile stones.
13.4.3.2 Cholestatic Changes/Inspissated Bile/Gallstone
Definition
Different causes, reactive either during infection due to medication (e.g. parenteral
nutrition, intensive care medicine, some antibiotics such as Ceftriaxone®), bile duct
obstruction by compression or tumours, intrinsic bile duct obstruction (stone and
sludge), functional impairment (cystic brosis, haemolytic anaemia, Hirschsprung
disease, etc.).
300
M. Riccabona
US Findings
• Variable dilatation of affected part (Fig.13.22).
• Potentially site of obstruction visualised.
• Sludge/stones within bile duct and gall bladder (Fig.13.23).
• Oedematous periportal eld, thickening of bile duct wall—if long standing or
chronic.
• Typical ndings in gallstones: Echogenic formation with more or less shadowing
depending on composition. Sludge—no shadowing, but sedimentation+ uid
levels. Cholesterol polyps are connected to gall bladder wall (DDx: gall bladder
wall polyps—polyposis, e.g. in metachromatic leukodystrophy) (see Fig.13.23).
Fig. 13.22 Dilated bile ducts: (a) Dilated main hepatic duct. (b, c) CDS helps differentiation of
portal vein from main hepatic duct
Fig. 13.23 Sludge and bile stones: (a) Normal gall bladder with sludge balls. (b) Sludge-lled
gall bladder with several small stones (increased echogenicity, partially with shadowing). (c)
Isolated infundibular bile stone (++) with shadowing. (d) Echogenic sludge in a dilated intrahepatic bile duct, some shadowing
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
301
Note In childhood, biliary stones are less common than in adulthood—should
prompt thorough search for underlying conditions (e.g. bile duct malformation, papillary stenosis, metabolic disease, haemolytic anaemia). Typical pitfall in diagnosing
calculi—air in adjacent bowel with associated shadowing or reverberations, echogenic vessel walls with side loop artefacts. And only some stones twinkle, some do not.
13.4.3.3 Sclerosing Cholangitis
Definition
Chronic cholestatic disorder, obliterative brosis of extrahepatic and intrahepatic
bile ducts, eventually leads to biliary cirrhosis associated with chronic inammatory
bowel disease and immune-deciency disorders.
US Findings
Typically thick-walled, dilated intrahepatic ducts with irregular shape and regionally secondary narrowing due to strictures.
Secondary cholelithiasis, intraductal stones, gall bladder wall thickening, devel-
opment of cirrhosis+portal hypertension.
Note Cholangitis in AIDS appears similar, but may have papillary oedema causing
hypoechoic nodule at distal end of common bile duct.
13.4.3.4 Other Forms ofCholangitis andCholecystitis
Rare in childhood, usually secondary to underlying condition, systemic disease (e.g.
Kawasaki disease) or postoperative.
US Findings
• Enlargement of gall bladder, thick bile duct and gall bladder wall, oedematous
gall bladder bed, periportal oedema and sludge formation (Fig.13.24).
a
Fig. 13.24 Thickened gall bladder wall: (a) Severely thickened gall bladder wall (++)—nonspe-
cic nding can be seen in a variety of conditions (e.g. congestion, hepatitis, Kawasaki, cholecystitis). (b) CDS depicts wall vessels; spectral analysis conrms its arterial nature with high-diastolic
hyperaemic ow and low resistance ow pattern, consistent with cholecystitis
b
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M. Riccabona
• In chronic, persistent or recurrent disease: complications from periportal brosis,
strictures, wall thickening, irregular contours and postinammatory
calcications.
• In tropic areas various parasites can ascend into bile ducts and cause inammation and obstruction—may sometimes be visualised moving within biliary tract.
Tip Validate obstruction+dilatation of bile ducts by US with valsalva-manoeuvre
(decrease of ductal diameter as positive response to manoeuvre in non-obstructed
biliary system) or by gall bladder size/duct size changes 30–60min after fatty meal
helpful.
CDS
Helpful to differentiate vascular from biliary structures, but only if performed at
adequate Doppler angle, hyperaemia/hypervascularisation of gall bladder wall vessels and hyperaemia of HA.
Note Arterial nature of vessel must be proven by spectral analysis—other condi-
tions may also cause increased vascularity of gall bladder wall (e.g. Henoch–
Schonlein purpura, Kawasaki disease, intensive care medicine with parenteral
nutrition, cardiac congestion and after resuscitation, portal hypertension, hepatic
vein obstruction).
13.4.3.5 Tumour-like Conditions
Polyps
Definition
Rare in childhood, associated with syndromes—particularly if multiple or numerous.
Should always be evaluated and followed up.
US Findings
• Usually quite homogenous echogenic formation, adjacent to bile duct/gall bladder wall, protruding into lumen (Fig.13.25). Stay at same side adjacent to wall
during positioning manoeuvres.
• Potentially exhibit central vascular pedicle on (a)CDS.
DDx: Concretion, brous, sludge/clot formation, “cholesterol polyps”, irregular
thickening or focal changes in inammation.
Multiple gall bladder polyps in metachrome leukodystrophy, practically
Note
pathognomonic.
Tumours
Cholangiocellular Tumours
Cholangiocellular tumours extremely rare in childhood. Rhabdomyosarcoma of bile
duct may occur—may show similar growth as cholangiocarcinoma.
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
Fig. 13.25 Gall bladder polyp. Gall bladder
polyp (++) attached to wall, stable in this
location during positioning manoeuvres. Similar
behaviour seen in the more echogenic
“cholesterol polyps” (DDx to stone formation that
moves and oats with manoeuvres)
303
US Findings
• Nonspecic. Tumourous lesion adjacent to central hilar structure, potentially
growing within dilated common bile duct, is causing intrahepatic dilatation of
bile ducts and cholestasis.
• May compress or affect hilar vascular structures, particularly PV.For differentiation biological markers and sectional imaging as well as biopsy are necessary.
Granular Cell Tumour
Benign tumour, rare, anywhere along biliary tree.
US Findings
• Echogenic, intraductal mass with secondary dilatation of respective part of biliary tree. Cannot be differentiated without histology.
13.4.3.6 Role ofUS
Cholestasis and Jaundice.
Initial investigation to differentiate various entities and nd dilatation of bile ducts.
Method of choice for depicting calculi, particularly in gall bladder and main/central
bile ducts.
Note If liver function and thus bile production impaired, even obstructed ducts will
not be dilated.
Malformations
Method of choice for rst investigation and follow-up.
Additional imaging depends on suspected condition.
Trauma
US restricted in early phase after trauma, but ideal for follow-up.
304
CDS usually helpful, particularly, when assessing HV/PV/HA complications,
aneurysms, stula, etc.
US potential signicantly enhanced by CEUS.
Postoperative Conditions
Particularly after Kasai-/Y-Roux Anastomosis—used to assess further course of disease. Cystic ectasia/dilatation of bile ducts may indicate some obstruction and stenosis at anastomotic site.
Secondary cholangitis, periportal brosis and aerobilia can be seen.
Metabolic Disease
Used to screen for liver involvement, insensitive for entity—usually shows unspecic changes of liver parenchyma and size. Multifocal inhomogenous patchy appearance may have irregular distribution, as also after various therapies (e.g. oncology).
US-Guided Biopsy (see also chapter Interventional US).
Helpful to reduce complications or for targeted biopsies of individual lesion.
Essential to secure safe needle tract with sufcient healthy liver tissue between
peritoneal cavity/skin and core biopsy site.
Helps reduce risk of complications: avoid major vessels, increase tissue harvest,
reduce number of passes, avoid injuring diaphragm/entering chest, penetrating into
abdominal cavity, etc.
M. Riccabona
13.4.3.7 Additional Imaging
• ERCP/MRCP: technically challenging in neonates and small infants; in narrow
bile ducts MRCP has insufcient resolution for visualisation/demonstrating
detailed anatomy.
• CT/MRI: for assessment of focal liver lesions that secondarily cause obstruction.
MR helpful in cholangitis, brosis and assessment of secondary liver tumours in
biliary cirrhosis. At present restricted role in diagnosing biliary atresia, not necessary for uncomplicated stone disease.
• Scintigraphy: Tc99m HIDA used in biliary atresia+liver function assessment.
• Interventional radiology: Punctures and drainages performed under US, uoroscopic or CT guidance. Used for relieve of obstruction, for cholangiography in
complex anatomy/biliary atresia, after trauma (bile leaks, collections, vascular
problems/embolisation), after transplantation (dilatation and stenting), for targeted biopsies of equivocal lesions or for abscess drainage.
13.5 US inLiver Transplantation
13.5.1 Pretransplant US
13.5.1.1 Recipient Evaluation
• Assessment of liver/focal lesions/initial diagnosis of liver disease.
• Documentation of patency of PV by CDS+spectral trace.
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
305
• Assessment of ascites and spleen (size).
• Demonstration of abdominal vascular anatomy, assessment of portosystemic shunts.
• Assessment of potentially associated renal disease.
13.5.1.2 Donor US (Split Liver Transplant, Related Living
Donor—Deceased Donor)
• In living donor: replaced by ce-CT or MRI, which allows reliable assessment of
parenchyma and (vascular) anatomy for exact planning.
• In deceased donor: US (to assess anatomy of PV, HV, vascular anatomic variations, presence of liver disease, etc.) or ce-CT (e.g. at same session with brain
CT/CTA when used for assessing brain death).
• Potentially 4Dce-US may widen US potential in future.
13.5.2 Intraoperative US
Not commonly used—sometimes for assessing vascular complications (difcult surgery, atypical anatomy, etc.) immediately before or shortly after abdominal closure.
13.5.3 Postoperative Assessment
US—mainstay of imaging, both in early and late stage.
Tasks of US
• Demonstrate anatomy and patency of vascular anastomosis (PV, HA, HV, IVC),
CDS+spectral analysis mandatory.
• Assessment and follow-up of focal collections (e.g. haematoma, haemorrhage,
biloma, secondary abscess formations).
• Assessment of bile ducts commonly only achievable in early phase after transplantation or with dilated ducts (stenosis, sludge, etc.). Otherwise periductal
brosis, aerobilia and calcications reduce US potential.
– Role of US elastography for evaluation of chronic transplant disease yet
unknown in children.
• US-guided drainage/biopsy potentially helpful.
Always include surrounding structures such as spleen, abdominal IVC (for
Note
patency and size), ascites, etc.
13.5.4 Typical Complications
• Vascular: HV occlusion, PV stenosis/thrombosis, HA stenosis/occlusion,
(pseudo-)aneurysm of HA, arteriovenous stula and liver infarction.
• Collections: abscess formation, haematoma, biloma and seroma.
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• Bile complications: bile leakage, bile duct stricture (commonly at site of
anastomosis), aerobilia, cholangitis, sludge and stone formation.
• Extrahepatic: ascites, splenomegaly, adrenal haemorrhage, pancreatitis,
lymphoproliferative disorders, IVC-thrombosis, pleural effusion, etc.
• Parenchymal disease: hypoxia, rejection and lymphoproliferative disorders.
Note US nonspecic. Diagnosis mostly made on clinical grounds, conrmed by
biopsy. Because of low sensitivity and specicity, role of US is to exclude other
graft complications and to detect early potential transplant tumours.
Common US Findings
• Heterogeneity of atypical parenchyma, e.g. in acute rejection or after
hypoxia.
• Monophasic hepatic vein waveform in all situations with increased liver resistance.
• Increased arterial resistance and pathology of ow proles (stenoses,
rejection, etc.).
• CEUS may help to evaluate vessel anatomy and patency (yet off-label).
• Intraluminal ce-US for cholangiography (as long as a drain is in place) may help
evaluating bile duct complications (presently off-label).
M. Riccabona
13.6 Spleen
13.6.1 Requisites
Usually curved linear arrays (and sector transducers) used.
For detailed analysis, linear transducers recommended.
Frequency adapted to age.
13.6.2 Positioning
Supine, prone, lateral decubitus.
Note Due to ribs examination can be unpleasant or tricky, thus cautious transducer
handling necessary.
13.6.3 Indications
• Enlargement of spleen—most common indication for abdominal US in
some areas:
– Huge variation in measurements, difcult to dene standard plane
– High inter−/intra-observer variations—of restricted reliability
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
307
• Involvement in systemic disease:
– Enlargement, focal lesions (abscess, fungus, lymphoma, leukaemia)
• Portal hypertension
• Trauma
• Haemolytic anaemia, thrombocytopenia, etc.
• Metabolic diseases, mucopolysaccharidosis, glycogenosis, etc.
• Malformations, syndromes (asplenia, polysplenia, etc.), etc.
13.6.4 Course ofInvestigation
• Find spleen in intercostal plane in left axillary line, sometimes deep inspiration
or “big belly” helps to visualise entire organ.
• Standardised measurements (coronal section with largest diameter/length that
includes the splenic hilar vessels).
• Assess entire organ in longitudinal+axial organ sections (see Table13.6).
• Always assess adjacent spaces: subphrenic and subsplenic/perisplenic.
• CDS helpful when looking for vessel pathology (e.g. posttraumatic aneurysm,
collateral and enlarged veins in portal hypertension, thrombosis/infarction, etc.).
13.6.5 Normal Anatomy
Normal spleen—inverted comma shape, larger surface positioned adjacent to left
diaphragm.
Large parallel vessels seen in hilus—follow into organ and to midline along
pancreas.
Homogeneous organ of rather low echogenicity with smooth margins and
rounded poles (Fig.13.26).
Table 13.6 Normal size of spleen depending on age/size and standard measurements
a
(a) Graph demonstrating standard measurements plains
(b) Maximal normal spleen length (mm) in neonates, correlated with body weight (kg)
(c) Normal spleen volume (mL) during childhood correlated to body height (cm). Volume calculated by normal ellipsoid equation (correction factor=0.5, average of depth measurement in two
planes used to reduce errors)
L=length, W=width and D=depth (in mm)
b
c
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M. Riccabona
Size—see age-adapted normal values (Table13.6), as rule of thumb: maximum
length (cm)=6+1/3 of age (years). Measurements taken in reproducible section
that includes hilar vessels:
• If spleen reaches lower third of normal sized and positioned left kidney = enlarged.
• In neonates shape and position of spleen different (more oblique).
13.6.6 Normal Variants
13.6.6.1 Splenunculus (Accessory Spleen)
Most commonly close to hilus (may be positioned anywhere), usually spheric or
ovoid, same echogenicity as splenic parenchyma, often some connection to spleen
with vascular hilus (arises from splenic vessels) (Fig.13.27).
Note Splenunculi may cause acute abdomen by torsion and infarction, often nota-
ble by lack of CDS signals. Sometimes difcult to differentiate from lymph nodes
(or real accessory spleen/polysplenia).
Fig. 13.26 Normal spleen. (a) Axial view. (b) Longitudinal view, with standardised section for
measurement (+ +): adequate section dened by hilar vessels, lower pole and upper pole
(medio-posterior)
Fig. 13.27 Splenunculus/splenule (accessory spleens). Small splenules in two different cases
(++) documented in axial (a) and longitudinal view (b)