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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5795_Библиотеки_им_академика_М_И_Перельмана.pdf
body
chol.
pancreatic
duct
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
319
13.7.4 Normal Findings
Echogenicity of pancreas changes with age:
• Newborn: pancreas rather hypoechoic, more spheric head, homogeneous echogenicity, smooth contours (Fig.13.36).
• Children: with age pancreas becomes increasingly echogenic with slightly stippled appearance, otherwise homogeneous parenchymal echoes.
• Commonly pancreatic echogenicity similar to liver—little higher than spleen. If
echogenicity increased—think of brosis, lipomatosis, haemosiderosis, medication and congestive changes. Shape of head and body similar to adults; tail often
slightly pronounced.
Measurements may be difcult, particularly in standardised planes—given val-
ues serve for orientation (Table13.8).
Pancreatic duct often seen, should not measure more than 1.5mm in older chil-
dren and 1mm in early childhood.
13.7.5 Variations andMalformations
13.7.5.1 Annular Pancreas
Difcult to see, lling duodenum with uid helpful.
Specic nding: circular shape of pancreatic head surrounding the usually com-
pressed and stenotic duodenum, with signicant change in calibre at that site.
Often associated with intrinsic duodenal obstruction (duodenal web, atresia, etc.).
13.7.5.2 Pancreas Divisum
Lack of fusion of ventral and dorsal part.
Rare normal variant.
Two different draining ducts that drain in papilla major/minor.
Table 13.8 Orienting values
for size of pancreas, and
where to take measurements
(a) Table for normal values of pancreas size during
childhood for orientation
Age
Newborns 0.5–1.0 0.5–1.1 0.5–0.8
0–6years 1.0–1.9 0.4–1.0 0.8–1.6
7–12years 1.7–2.0 0.6–1.0 1.3–1.6
13–18years 1.8–2.2 0.7–1.2 1.3–19
(b) Schematic drawing illustrating standard sections
for measurements of head, body and tail thickness,
chol.duct=choledochal duct
duct
Head
(cm)
head
Body
(cm)
Tail
(cm)
tail
320
M. Riccabona
US Findings
• Two plate-like bars of typical echogenicity tissue separated by anechoic platelike layer.
• Variation of pancreatic duct system—not reliably assessable by US.
13.7.6 Inflammation: Pancreatitis
Pancreatitis usually primarily a clinical/serologic diagnosis.
Different entities.
13.7.6.1 Oedematous or Reactive Pancreatitis
Commonly seen in viral infection, may also occur posttraumatically.
US Findings
• Enlargement and swelling with more spherical appearance (Fig.13.37a, b).
• Can be restricted to just body or tail (Fig.13.37c, e).
• Commonly slightly changed texture, often hypoechoic—may more prominently
delineate pancreatic duct. May also be of increased echogenicity (particularly if
combined with underlying or recurrent disease) (Fig. 13.37d) or patchy
(Fig13.38a).
• Depending on amount of exsudation, there can be peripancreatic uid
(Figs.13.37d and 13.38b).
• Hazy border to affected neighbouring mesentery and surrounding structures that
reactively become more hyperechoic.
13.7.6.2 Haemorrhagic or Necrotising Pancreatitis
US Findings
• Swelling, increased size.
• Inhomogeneous, patchy, even hyperechoic echotexture.
• Potentially focal lesions with hyper- or hypoechoic appearance (haemorrhage,
necrosis, etc.).
• Secondary pseudocyst formation (often later during course of disease).
• Secondary abscess formation.
• Calcications and haemorrhage possible (Fig.13.39).
• Usually signicant exsudation with free uid around pancreas and other abdominal compartments (Fig.13.37d, Fig13.38b).
• Pleural effusion.
• Always assess ductal system including bile duct (bile obstruction as cause for
infection?).
• Consider trauma as potential reason.
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
321
Fig. 13.37 Acute pancreatitis. (a) Swollen, enlarged and hypoechoic pancreatic head in acute
(viral) pancreatitis, axial section. (b) Swollen and enlarged pancreatic head (++
pancreatitis, sagittal section. (c) Prominent and slightly irregular duct in tail and body of enlarged
and inamed pancreas. (d) Exsudation along left kidney in severe exsudative pancreatitis
a
Fig. 13.38 (a) Irregular patchy structure of swollen pancreatic tail in pancreatitis. (b) Severe
exudation around the head of the pancreas—in posttraumatic pancreatitis
b
1
) in acute (viral)
13.7.6.3 Chronic Pancreatitis
Rare in childhood.
Potentially secondary to systemic disease (e.g. CF, choledochal cyst,
metachromatic leukodystrophy), also familial can be recurrent.
322
Fig. 13.39 Chronic pancreatitis. (a) Parenchymal calcications in pancreatic tail in chronic recur-
rent pancreatitis with irregular and enlarged pancreatic duct, accessed via uid-lled stomach. (b)
Echogenic swollen pancreatic head in chronic recurrent pancreatitis (CF-patient)
M. Riccabona
US Findings
• Irregular contour, increased echogenicity.
• Regional calcication (Fig.13.39a).
• Irregular size of potentially enlarged pancreatic duct/subducts (Fig.13.40).
• Potentially secondary stenosis.
• With increasing duration—atrophy and lipomatosis, secondary necrosis, pseudocysts (Fig.13.41).
13.7.7 Trauma
In childhood possibly affected in blunt abdominal trauma:
• Particularly in accidents with bicycles (handlebar injury).
• Furthermore seen in abuse and vehicle trauma (seat belt injury).
US Findings
Vary with severity and kind of injury, grading see Table13.9:
• Nonspecic swelling in area of contusion with regionally altered echotexture.
• Superimposed ndings of reactive pancreatitis.
• Rupture/haematoma seen as disruption of contour/structure by focal initially
echogenic, later on anechoic or hypoechoic inhomogeneous structural disruption
(Fig.13.42).
• Potential leak of pancreatic exudate if ducts involved.
• Secondary necrosis, formation of pseudocysts.
• Peripancreatic uid.
ab
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
Fig. 13.40 Irregular dilated pancreatitic duct. (a) Enlarged and irregular pancreatic duct in body
1, 2
(++
) in an infant with recurrent pancreatitis. (b) Hazy hypoechoic pancreatic parenchyma with
irregular ductal ectasia in pancreatic tail as well as stippled calcication in the body—in acute
exacerbation of recurrent pancreatitis
Fig. 13.41 Pancreas pseudocyst. Large complex
(pseudo-)cyst (++) in body and tail of pancreas,
axial view
323
Table 13.9 Grading of pancreatic injury (according to Lucas)
Grade I Supercial contusion, no involvement of ducts
Grade II Peripheral rupture, rarely a peripheral duct involved, distal parts of pancreas involved
Grade III Proximal rupture or even burst, duodenum not involved, pancreatic duct may be
Grade IV Complex injury of pancreas, duodenum, pancreatic duct and potentially choledochal duct
involved
These changes often only depicted on follow-up, particularly increasing amount
of uid surrounding pancreas, delineation of necrosis and development of pseudocysts—usually only after days.
Note US can guide drainage of pseudocyst, but only advisable after solid and well-
formed cyst wall established.
13.7.8 Space-Occupying Lesions
13.7.8.1 Cysts/Pseudocysts
Most common—congenital (systemic cystic disease), posttraumatic and
postinammatory.
324
ab
c
Fig. 13.42 (a) Pancreas laceration. Subtle irregularity of pancreas contour at junction between
head and body ventrally after trauma (b) Pancreas laceration in typical location, in (c) also with
signicant perifocal oedematous and exudative reaction
M. Riccabona
US Findings
• Simple cysts—anechoic, spheric structure, thin and smooth wall.
• Complicated (pseudo-)cysts: often contain anechoic uid potentially with some
debris, echoes, sedimentations and septae. Wall often irregular, polygonal—
appearance varies with origin and age of cyst—may grow and become very large
(see Fig.13.41).
Cysts often accessible for US-guided puncture/drainage.
13.7.8.2 Tumours
Extremely rare in children. Different entities:
• Adenoma, hamartoma and insulinoma:
– Focal tumour.
– Diffuse “inltration”—nesidioblastosis—hyperplasia of insulin producing
beta cells.
• Rarely adenocarcinoma.
• Solid-pseudopapillary semimalignant tumour=Frantz tumour (Fig.13.34).
• Involvement in leukaemia/lymphoma (Fig.13.43).
• Focal granulomatous pseudotumour—may be difcult to differentiate (involve-
ment in HIV, sarcoidosis, tuberculosis, etc.) (Fig.13.43).
Assess for secondary changes (e.g. obstruction of pancreatic/bile duct, local
Note
spread to duodenum, regional lymph nodes and involvement of PV/coeliac trunk/
splenic vein/mesenteric artery). Also consider that US may miss small tumours, particularly if of similar echogenicity as normal pancreatic parenchyma, or diffuse inltration.
US and (a)CDS Findings
• Focal tumourous disruption of typical echotexture with regionally increased size,
commonly anechoic or less echogenic than parenchyma.
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
325
ab
Fig. 13.43 (a) Pancreatic pseudotumour in HIV-infected girl (DDx: lymphoma). Hypoechoic
tumourous lesion in body of pancreas (axial view), which turned out to be an inammatory pseudotumour in a girl with HIV and pancreatic tumours: small and hypoechoic lesion (+…+) in the
pancreatic tail, slightly difcult to depict on US (b, lymphoma) with regional lymph nodes (×…×),
and large heterogenous and partially cystic tumour in the head of the pancreas (c, Frantz tumour)
c
• Depending on aetiology—sharp or hazy, irregular margins.
• CDS rarely helpful. May help differentiation of tubular ectatic ductal struc-
tures from vessels or vascular pathology, or to assess patency of vessels
(secondary thrombosis—e.g. of splenic vein and aneurysm of adjacent
arteries).
• Depiction can be improved by aCDS, ce-US, endoscopy/endoscopic US and
intraoperative US (helpful for location during surgery).
13.7.9 Role ofUS
Commonly used as rst imaging modality:
• Always evaluate pancreatic US in conjunction with laboratory ndings.
Note Morphologic changes may manifest later than disease onset.
Also used for follow-up, intraoperatively and for guiding interventions.
Sometimes subtle (traumatic) lesions better seen than on CT—for
resolution issues.
13.7.10 Additional Imaging
• Sectional imaging by MR (or CT) helpful, particularly in trauma or for tumour-
ous conditions.
• CT mandatory in severe trauma for early depiction of frequent associated inju-
ries of bowel or bony structures.
• Scintigraphy/PET in some tumours, inltration, nesidioblastoma, etc.
• ERCP offers best anatomic resolution for assessing pancreatic duct; MRCP
(sometimes performed with secretin) presently useful only in obvious/gross
dilatation.
326
M. Riccabona
13.8 Retroperitoneum andRetroperitoneal Structures:
Abdominal Vessels andAbdominal Wall
13.8.1 Abdominal Vessels
13.8.1.1 Positioning
Usually assessed in supine position, using topographically dened access from ventral or lateral, depending on position of investigated vessel.
13.8.1.2 Transducers
Depends on position of vessel and patient age as well as size of patient.
Try to use linear transducers for high-resolution anatomic assessment,
particularly in neonates, infants and slim children.
Curved arrays preferred with slightly lower frequencies for optimal Doppler.
Note For detailed Doppler studies, good Doppler angle (<60°) essential for reliable
measurements. Patient motion as well as overlying gas may often hinder continuous
visualisation of main abdominal vessels, particularly in middle and lower abdomen
as well as pelvis.
13.8.1.3 How toInvestigate
Usually vessel assessed in longitudinal and cross section, including not only vessel
wall and position but also main branches. Always consider normal variants/variations
that may hint at underlying congenital malformation/syndrome (e.g. persisting
left IVC).
Note Graded compression may be necessary for access—but may cause
“pseudopathology”.
13.8.1.4 US Findings
Typically vessels have echo-poor lumen. With high-resolution transducers, oating
particles may become visible. Venous wall thin, arterial wall thicker with muscular
layer and more or less pulsation.
Note Physiologic changes in calibre of abdominal aorta after descending distal to
major upper abdominal parenchymal vessels (coeliac trunk, mesenteric artery, renal
arteries). Similar phenomenon seen in IVC—often larger proximal to renal vein
insertion than distally. Pronounced changes in calibre may hint towards focal steal
phenomena, e.g. by hyperperfusion of specic organ system (e.g. high ow haemangioma/haemangioendothelioma with signicant tapering of abdominal aorta
distal to coeliac trunk) (Fig.13.44).
Anatomy and pathology of various organ vessels described in their respective
chapters—numerous normal variants.
ab
13 Upper Abdominal US inNeonates, Infants andChildren: (Excluding the Kidneys)
327
cd e
Fig. 13.44 Major abdominal vessels—normal ndings. Schematic drawing of normal important
arterial (a) and venous (b) abdominal vessels. Typical normal US appearance of major abdominal
vessels, sagittal section: (c) inferior vena cava (IVC, × … ×), (d) upper abdominal aorta and
branching superior mesenteric artery (arrowheads) and coronal view using power Doppler demonstrating aortic bifurcation (e)
CDS
Aorta: typical high-resistive ow patterns with triphasic modulation and negative
early diastolic phase observed.
Peripheral/main arteries of major abdominal organs: low-resistive organ ow
pattern observed, typical high antegrade diastolic ow. Variations with splanchnic
activation are seen in coeliac trunk and superior mesenteric artery.
Venous: biphasic and even bidirectional modulation by cardiac action and
respiration.
13.8.1.5 Important Variants andMalformations
• Azygos continuation/double IVC, inverted situs (aorta to right, IVC to left).
• Malposition of mesenteric vessel (see also chapter on bowel US).
• Narrow origin of superior mesenteric artery by compression from crossing
duodenum.
• Narrowed (or retroaortic course of) left renal vein with consecutive clinical
obstructive symptoms (see chapter on urogenital US).
Note Graded compression may be needed for removing gas and getting sufcient
sonographic access—but this technique may also compress vessels and thus
decrease depictability, or cause artefactual pseudo-stenotic ow patterns.
328
M. Riccabona
13.8.2 Vascular Pathology
13.8.2.1 Thrombosis/Occlusion
General Remarks and US Findings
Thrombosis/embolus: echogenic material within lumen, lack of ow on CDS, if
accessible incompressible distended lumen; in long-standing thrombosis revascularisation (of wall as well as thrombus), secondary calcications occur. In tumour
thrombus sometimes vascularisation of thrombus by tumour vessels.
Note Assessment of mesenteric vessels and central renal/splenic vein difcult—no
possibility to rule out thrombus or occlusion, particularly if more distally.
Thromboses occur in pelvic veins, renal veins, potentially also IVC and aorta
(e.g. embolic after cardiac or umbilical artery catheterisation).
Causes: central lines, coagulopathies, compression, but also typically for Wilms’
tumour and tumour invasion in renal vein (may progress to right atrium through
IVC). Can usually nicely be depicted by US and CDS (Figs.13.44 and 13.45); sensitivity sometimes better than of other sectional imaging:
• Missing or occluded IVC most often depictable by large paravertebral collateral
vessels or venous plexus that drains into deeper compartments—try to follow pel-
vic veins to dene normal insertion into normal distal IVC—here lateral access or
access through well-lled large bladder helpful, as well as “graded compression”.
Note Dene cause of obstruction; evaluate patency of pelvic vessels.
abc
ed f
Fig. 13.45 Thrombosis in large abdominal vessels. (a, b) Left pelvic vein thrombus, (a) longitu-
dinal, (b) cross section: no colour signals in large, incompressible pelvic vein (++). (c) Calcied
rim-like echogenic border around old IVC thrombus (cross section), no colour ow. (d) Embolic
thrombus to abdominal aorta (arrowheads) subacute plevic vein thrombus seen as inhomogenous
lling of the incompressible vein in longitudinal and axial section (e, f)