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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5795_Библиотеки_им_академика_М_И_Перельмана.pdf
15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
411
Note Always assess all renal sectors (as in children intrarenal stenosis quite com-
mon)—peripheral and main segmental branches need to be seen on CDS for reliable
assessment. Always assess abdominal aorta/other low-resistive ow vessels (e.g.
coeliac trunk, cerebral vessels) to differentiate focal from systemic conditions.
Remember, that particularly in gray scale dissection may be hard to see; US does
not always allow exclusion of stenosis. In some conditions ce-US can enhance US
potential.
Additional Imaging
Captopril scintigraphy.
CT/MR angiography and catheter angiography with PTA/stenting.
15.3.3.2 Arteriovenous Fistula (AVF)
Definition
Rarely spontaneous or idiopathic (vasculopathies), common after surgery,
trauma, biopsy.
US Findings
Large stula may show as cystic interruption of normal renal parenchymal structure.
Secondary sedimentation in renal pelvis due to haemorrhage.
Cortical infarct of dependent area.
CDS
Most useful tool for depicting AVF.
• Adapt scale to become sensitive for aliasing (demonstrates site of AVF).
• Feeding artery hyperaemic with increased velocities/low RI; draining vein may
have increased velocities with arterialised ow spectrum—spectral analysis
mandatory (see Fig.15.35).
• At AVF: unidirectional high-velocity turbulent ow.
• aCDS visualises focal peripheral perfusion impairment of dependent areas—risk
of infarction.
Additional Imaging
ce-CT/MRA.Catheter angiography—potentially with embolisation.
15.3.3.3 Infarction
Definition
Rare in childhood—posttraumatic, postoperative, postinterventional, in coagulopathies, other systemic disease such as haemolytic anaemia (e.g. sickle-cell anaemia).
US Findings
Initially difcult to differentiate from focal pyelonephritis but soon develops
increasingly sharp borders with triangular shape and rather echogenic parenchyma
(Fig.15.29).
412
M. Riccabona
abc
Fig. 15.29 Renal infarction. (a) Echogenic, more or less triangular-shaped segmental parenchy-
mal lesion in a child with sickle-cell anaemia, consistent with an infarction. (b) No vessels depictable by aCDS in this traumatic renal infarction of parts of the kidney (dissection of supplying
accessory artery). (c) Polar infarction (++) demonstrated by aCDS after sacricing a polar artery
during transplantation
Eventually (necrosis) less echogenic, develop into scars—cannot be differentiated from other scars.
aCDS
Segmental perfusion defect; detection can be enhanced by intravenous ce-US.
Additional Imaging
Only if of therapeutic consequence: ce-CT/MRI.Potentially scintigraphy.
15.3.3.4 Renal Vein Thrombosis
Definition
Rare, but exists even in neonates:
• Causes: posttraumatic, postoperatively, postinterventional, coagulopathies,
dehydration, systemic infection, tumourous/by local compression/displacement
(e.g. after neonatal adrenal gland haemorrhage with displacement of kidney—in
this condition always assess renal perfusion!).
• May often start peripherally, eventually grows into central veins—in early stages
central renal vein may be patent.
• Tumour thrombus (particularly Wilms tumour) may grow through renal vein into
IVC, up to right atrium. Risk of pulmonary embolism.
US Findings
• In central vein or IVC, thrombus formation is visualised replacing normal
anechoic lumen of then often distended vessel.
• Most striking—secondary changes in the kidney: swollen, echogenic (regionally
pronounced= haemorrhage) and with disrupted cortico-medullary differentia-
tion (Fig.15.30).
• Intrarenal thrombus cannot be visualised directly.
abc
15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
Fig. 15.30 Renal vein thrombosis—typical US and CDS ndings. (a) Echogenic swollen kidney
in neonate with haematuria. (b) CDS with spectral trace exhibits high-resistance arterial ow; no
venous ow depictable. (c) Renal vein thrombus reaches into IVC
413
CDS
• Striking hypovascularisation of affected area/kidney; non-affected parts/central
vessel may still exhibit antegrade ow (often with bidirectional colour ow sig-
nals) (Fig.15.30).
• Spectral trace in affected area—bidirectional arterial ow with short high-peak
systolic inow and diastolic backow, which drains all systolic blood ow (no
effective antegrade perfusion).
• No venous colour signals/ow spectra depicted in affected area/vein(s).
Role of US
In combination with clinical symptoms and signs, the typical US and CDS ndings
are diagnostic; no additional imaging needed or will reveal additional information.
Even in tumour thrombus, CDS is the most sensitive method; otherwise for assessment of thrombus of IVC, contrast-enhanced sectional imaging may be used.
15.3.4 Nephrocalcinosis
Definition
Precipitation of echogenic, calcium containing material at cortico-medullary junction, tubules/papillae, cortex….
Various causes: hypercalciuria, distal renal acidosis, Bartter syndrome, oxalosis,
secondary to other diseases (e.g. sickle-cell anaemia/sickle-cell nephropathy).
US=major imaging tool.
US Findings
Sonographically medullary nephrocalcinosis exhibits three stages (Fig.15.31):
• Stage I: initially echogenic cortico-medullary transition zone.
• Stage II: increasing peripheral medullar echogenicity, increasing echogenicity of
papilla—eventually entire medulla echogenic. DDx of latter: remnant of papil-
lary necrosis.
414
Fig. 15.31 Nephrocalcinosis. (a) Echogenic depositions in distal tubules close to papillae in a
neonate after furosemide therapy. (b) Echogenic outer layer of medulla in early (stage I) medullary
nephrocalcinosis. (c) Entire medullae calcied, with shadowing—late stage of medullary nephrocalcinosis (stage III), but cortex is preserved (no global calcinosis)—kidney borders difcult to
depict, outlined (++
1, 2
)
M. Riccabona
• Stage III: entire medulla calcied; nally also cortical deposits—increasing
echogenicity of the entire kidney.
Note Commonly nephrocalcinosis starts at medulla, not to be confused with physiologic transient medullary/papillary echogenicity of neonates (transient, resolves
spontaneously).
Cortical forms initially cause increasing echogenicity of cortex (e.g. overdose of
Vitamin D).
Global nephrocalcinosis of cortex + medulla extremely rare in childhood,
often late stage of systemic disease, with additional urolithiasis/papillary necrosis, etc.
CDS
Twinkling sign—particularly in more advanced forms.
Role of US
• Mainstay of imaging.
• Depicts ndings in early stage (still negative on plain lm).
• Also used for follow-up.
• CT will also show deposit but not used due to radiation burden.
DDx
Similar gray scale ndings in atypical manifestation of congenital nephrotic syndrome of Finnish type, ARPKD, renal vein thrombosis, cystinosis, oxalosis, glycogenosis, and tyrosinemia—these conditions must particularly be considered with
atypical manifestation, visualising of other signs (e.g. tubular ectasia) and very
early manifestation. Can eventually also lead to calcication of papillae (papillary
calcinosis) and urolithiasis.
15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
415
a
c
Fig. 15.32 Urolithiasis. (a) Stone with shadowing in proximal ureter/pelvi-ureteric junction.
Kidney enlarged (+…+) and hyperechoic in acute obstruction by urolithiasis; some dilatation due
to recurrent episodes larger than usually seen in single acute event. (b) Same patient as in (a):
subtle twinkling of stone—not all stones exhibit vivid twinkling. (c) Stone (
ing in mid-ureter—note change of calibre of ureter due to obstruction; ureter visible by using
graded compression following psoas muscle. (d) The twinkling sign depicts stone in proximal
ureter, hard to see on gray scale US (little shadowing and only slight distension of collecting system). Kidney swollen, hyperechoic, with vague cortico-medullary differentiation in peri-acute stage
b
d
+…+) with shadow-
1
15.3.5 Urolithiasis
Definition
Less frequent in children than in adults—varying geographic distribution.
Number of underlying metabolic conditions to be considered.
Details of US appearance/value of additional imaging are partially described
above (nephrocalcinosis), partially illustrated in Fig.15.32.
Most stones can in childhood be depicted sonographically—thus “stone-CT” is
rely needed in childhood and should be avoided for radiation issues (particularly as
stone disease often is a life-long condition that will cause many repetitive CTs later
on in adulthood, and radiation burden will add up over time to considerable doses!).
However, a full bladder and meticulous scanning is essential for not missing particularly distal ureteric stones.
US/CDS/Doppler Findings (Fig15.32)
Stone can be more or less echogenic, depending on the composition
• Often with shadowing—but not always
Kidney enlarged/swollen.
416
M. Riccabona
Parenchyma hyperechoic in acute obstruction/(hyper-)acute stage, with vague
cortico-medullary differentiation
Little dilatation of pelvi-caliceal system in acute event
• More distention in recurrent episodes or with preexisting dilatation
Twinkling sign on CDS, but not all stones exhibit vivid twinkling.
• May help to depict stones (e.g. in non-dilated proximal ureter) which are hard to
see on gray scale US
Asymmetrically elevated RI in affected kidney (in acute stage)
• Will gradually normalize over time even if stone not resolved (as in obstructive
uropathy—see respective entry)
Usually stones sit at pelvi-ureteric junction or distal ureter just before ureterovesical junction, then easily accessible in most (pediatric) patients
• Sometimes different locations (e.g. pelvic vessel crossing)—the latter approach-
able by gradually following the slightly distended proximal ureter without too
much compression to the level pelvic entry. These stones sit close to common
iliac vessels and next to the iliopsoas muscle—then often the caliber change and
the echogenic twinkling stone can be visualized
Bladder inow jet (best seen by CDS) may be missing or asymmetric
• Sometimes stronger on affected side due to erythrocytes as strong reectors in
urine from affected side thus increasing color signals
If some echogenicities cannot be properly located, try positioning maneuvers
Tip
to differentiate papillar or wall calcications/structures from intraluminal oating
stones that move when repositioned.
Note Do not confuse physiologic conditions with stones or nephrocalcinosis—e.g.
the physiologically echogenic papilla of the newborn that also may even cause twinkling, air in the system (e.g. after surgery or intervention or if reuxing after catherization), or e.g. fungus balls
US used for follow-up, but remnants of urolithiasis after lithotripsy will appear
different as the original stone.
With increase in nephrocalcinosis, visualisation of urolithiasis within collecting
system and differentiation of urolithiasis versus papillary calcinosis will become
difcult.
15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
417
Additional Imaging
Abdominal plain lm (KBU)—in some places still standard in imaging
urolithiasis,
• May be necessary for deciding on treatment or guiding percutaneous shock wave
lithotripsy
IVU (intravenous urography) in general practically outdated—only sometimes,
in special cases, focused IVU with selected images and timing may be the easiest
and only available problem-solving tool
• Particularly in (e.g. remote) areas with restricted access to dedicated pediat-
ric imaging
In children rarely unenhanced (low dose) stone CT indicated (reasoning
see above)
Mostly used as problem-solving tool in equivocal cases
• And in patients not suitable for US (e.g. obesity, spine malformations with dis-
torted habitus and lacking sonographic access, etc.)
MRI not well established for this query and also has restricted potential
15.3.6 Other Important Renal Parenchymal Disease
15.3.6.1 Haemolytic Uremic Syndrome (HUS)
Definition
Complication of bacterial enterocolitis; haemolysis congests renal vessels—causes
renal failure.
US Findings
Initially bilateral enlarged hyperechoic kidneys with small anechoic medullae.
Three stages differentiated:
• I: increased cortical echogenicity in relation to adjacent liver.
• II: even more increased echogenicity—still small hypoechoic medullae
visible.
• III: completely hyperechoic kidney without cortico-medullary differentiation;
always associated with complete renal failure.
Further development depends on course of disease—from stepwise normalisation to cirrhotic kidneys with chronic renal failure (CRF).
418
M. Riccabona
CDS
• Nonspecic but helps to nd vessels for spectral analysis.
• Signs of increased resistance with low/inverted diastole, high systolic ow, and
increased RI.
• Reduced venous ow.
Note Doppler nonspecic. Always assess other vessels for comparison (renal ver-
sus systemic/cardiac condition).
Tip Spectral analysis may help predict prognosis—perfusion patterns normalise
prior to normalisation of creatinine on blood samples, helpful in planning ongoing
dialysis.
Additional Investigation
• Always assess entire abdomen—conrm diagnosis of enterocolitis.
• Search for ascites/other complications.
• Eventually—in unclear cases/prognostic reasons—US-guided renal biopsy (pro-
vided normal coagulation).
• No other imaging performed.
15.3.6.2 Glomerulonephritis/Nephrotic Syndrome
See above.
15.3.6.3 Scars, Cirrhotic Kidney
Remnants or residual of previous disease.
Cirrhotic kidney always associated with severe loss of renal function. If other
kidney healthy—contralateral hypertrophy (volume calculations essential).
Focal scars: usually after trauma or infection and infarction, dened by parenchymal narrowing, calyceal clubbing, altered echogenicity, and cortico-medullary
differentiation—also see above. Focal hypertrophy—hypertrophic Bertin
columns.
US/CDS Findings
• Diffusely/focal altered echogenicity, variably clubbed calyceal system.
• Commonly increased echogenicity with reduced cortico-medullary differentiation.
• Focal or diffuse reduced vasculature—however, RI may be normal.
Additional Investigations
• DMSA scintigraphy for split renal function (results with function <30% less
accurate).
15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
419
• IVU outdated.
• If aetiology unclear, consider VCUG/ce-VUS (if of therapeutic consequence).
• Increasingly MRI used for assessment of kidney/calculating split renal function.
15.3.7 Renal Failure (RF)
Definition
Acute or chronic, persisting or transient.
• Prerenal: systemic condition that impacts renal perfusion/function.
• Intrarenal: disease affecting renal parenchyma, also involvement of renal paren-
chyma in systemic disease (e.g. lupus).
• Postrenal: commonly severe obstructive uropathy.
US Findings
• Acute pre-/intrarenal failure exhibits large, swollen, echogenic kidneys+altered
cortico-medullary differentiation.
• Findings depend on age, severity, and underlying disease.
• In polyuric phase, collecting system may be distended.
• In anuria collecting system collapsed.
• In chronic obstructive uropathy: dilated system.
• Chronic renal failure (CRF) depends on underlying disease—no specic ndings.
CDS
Particularly in early acute phases (asymmetrically?) elevated RI with low diastolic
ow. In chronic failure RI pseudonormal, with low ow velocities.
Role of US
Method of choice for initial diagnosis, follow-up, and differentiating different kinds
of renal failure.
15.3.8 Renal/Urinary Tract Trauma
Grades (Table15.4) with respective US Findings:
• Perirenal/subcapsular haematoma: intermediate homogeneous echogenicity,
may be difcult to differentiate from cortex. With duration increasingly
hypoechoic with sedimentation/clot formation, situated either subcapsular
(maintains shape of kidney) or perirenal. aCDS particularly valuable for early
stages, where gray scale may miss even signicant haematoma.
420
Table 15.4 Renal injury grading system (American Association for the Surgery of Trauma)—
according to depth of damage and involvement of the urinary collecting system and renal vessels
Grade I Contusion or non-enlarging subcapsular haematoma, no laceration
Grade II Supercial laceration <1cm depth
Does not involve collecting system
Non-expanding perirenal haematoma
Grade III Laceration >1cm
Without extension into renal pelvis or collecting system
With no evidence of urine extravasation
Grade IV Laceration extends to renal pelvis or urinary extravasation
Grade V Shattered kidney; devascularisation of kidney due to hilar injury
M. Riccabona
• Contusion: regionally altered parenchymal structure with increased echogenicity,
sometimes only seen after several hours. Even in early phases focally altered
vascular architecture on aCDS.Well seen on ce-US.
• Laceration: initially sometimes difcult to depict due to same phenomena as
above; may be improved by aCDS/ce-US.Always associated with perirenal haematoma, disruption of capsule, varying amount of retroperitoneal haemorrhage
and haemoperitoneum. Always try to assess whether major central structures are
affected (vessels, collecting system)—aCDS essential.
• Traumatic haematuria: only indirect signs (echoes within collecting system,
clots, disruption/thickening of pelvic wall)—US less sensitive, maybe ce-CT/−
MR necessary.
Note In children, haematuria not predictive for kind, severity, or prognosis of
renal injury!
• Hilar dissection: kidney looks sonographically normal. Only CDS reveals lack
of perfusion of kidney and disruption/alteration of ow at dissected/disrupted
vessel. Transection or disruption of ureter difcult to visualise—only depicted
by indirect signs such as urinoma formation.
• Posttraumatic changes: haematoma often resolve spontaneously, urinoma may need
drainage of collecting system (do not drain urinoma itself!). Secondary scars, complex cysts, calcications, posttraumatic aneurysm/AVF, shrinking kidneys, etc.
Role of US
• First investigation in emergency room (FAST).
• Detailed US study in mild/moderate urinary tract trauma (always include CDS)
(Fig.15.33).
• Method of choice for follow-up in most of conservatively treated patients (see
ESUR/ESPR recommendations for imaging childhood renal trauma—Pediatr
Radiol (2011) 41:939).
Additional Investigations
• In acute severe (poly)trauma=ce-CT.
• For follow-up, in complex/subacute situations=MRI.