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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5790_Библиотеки_им_академика_М_И_Перельмана.pdf
10.2 Normal Findin gs
327
a
b
cde
Table 10.1 Renal size – normal values (according to Weitzel) (a) Schematic drawing of longitu-
dinal renal section and axes for renal size measurements, l length, w width, d depth. (b) US image
axial section from left fl ank: cross section at hilus, orthogonal diameters for volume calculation (+
) and US image of a newborn kidney (right fl ank); longitudinal section: length measurement
.... +
1,2
(callipers) for volume calculation (c) Renal size (volume) in newborn (ml) versus body weight (kg)
( d) Normal renal volumes (ml) for left kidney related to body weight (kg) (e) Normal renal volumes
(ml) for right kidney related to body weight (kg)
abc
de
Fig. 10.5 Normal aCDS of kidney. ( a ) CDS of main renal vessels – median ventral access: left
renal vein ( red ) running in front of renal artery (encoded in blue ) and passing anteriorly to abdomi-
nal aorta. ( b ) Further normal course of left renal vein ( arrow ) between abdominal aorta and supe-
rior mesenteric artery till entering inferior vena cava (IVC); due to some narrowing increased fl ow
velocity and some fl ow turbulence causing aliasing on CDS. ( c ) Accessory renal arteries, which
can be a normal variant, but may also be associated with urinary obstruction due to vascular
impairment of proximal ureter/pelvi-ureteric junction. ( d ) Normal aCDS of a healthy kidney –
axial section. ( e ) Normal duplex trace of main/segmental renal artery
328
10 Ultrasound of the Urogenital Tract
ab
Fig. 10.6 Retro-aortal left renal vein. ( a ) Abnormal course of left renal vein accessed through
kidney from a longitudinal (coronal) fl ank view: blue-coded vein courses distally instead of run-
ning cranially parallel to renal artery. Note some aliasing at the area the vein reaches abdominal
aorta. ( b ) Ventral median axial view: left renal vein (encoded red ) passes behind abdominal aorta
with tapering due to some compression between aorta and vertebral body
10.2.2.1 Normal Variants
Number of variations that do not necessarily indicate pathology: parenchymal
bridge/hypertrophic column of Bertin in duplex kidney, rotation/position anomalies, caliectasia, extrarenal pelvis, persisting renunculae, other contour alterations
(e.g. “splenic bump”), variations in vessels such as accessory renal arteries/veins
and retroaortic left renal vein (Fig. 10.6 ).
Duplex Kidney
US Findings
Central parenchymal bridge, sometimes disproportionate upper and lower collecting systems, potentially associated dysplasia with lack of cortico-medullary differentiation and increased echogenicity commonly of upper pole moiety parenchyma
(Fig. 10.7 ):
• Obstruction most commonly in upper system, rarely involves lower pole
system.
• Meyer - Weigert rule – ureter of lower system drains latero-cranially into
bladder with risk of VUR, whereas ureter of upper pole system usually drains
distal- medially, may even insert ectopically, may be associated with ureterocele and often is obstructive.
• Lower system usually refl exes (refl ux nephropathy? secondary obstruction/
kinking?).
Always try to assess whether there is one common extrarenal pelvis or two ureters
leaving kidney; also try to visualise precise ostial anatomy (1 or 2 ostia? 2 jets? etc.).
Ectopic Kidneys
US Findings
May be anywhere in the retroperitoneum, may be small and dysplastic, sometimes
only cystic remnants are seen. Even intrathoracic position possible – then close to
diaphragm and paramedian dorsally (Fig. 10.8 ).
10.2 Normal Findin gs
a
bc
de
Fig. 10.7 Duplex kidney. ( a ) Duplex kidney (+…+2), longitudinal fl ank view: no distension of
renal collecting system, only parenchymal bridge in middle of kidney (
pelvis echoes indicates duplication. ( b ) Duplex kidney, longitudinal fl ank view: disproportional
dilatation of lower collecting system. ( c ) Duplex kidney, longitudinal fl ank view tilted medially:
two separate ureters of upper and lower moiety seen, with different grade of distension of respective collecting system. ( d ) Duplex kidney, longitudinal fl ank view: signifi cant dilatation of upper
moiety with unstructured, narrow, echogenic parenchyma; lower moiety exhibits normal parenchymal structure: NOTE: signifi cantly reduced vascularity on aCDS in dysplastic upper moiety. ( e )
Huge, cystiform dilatation of upper moiety of duplex kidney with rim-like residual dysplastic
parenchyma, only slight dilatation of lower system - not to be mistaken for a renal cyst
+ …+) interrupting central
1
329
ab
Fig. 10.8 Ectopic kidney. ( a ) Pelvic ectopic kidney (+ +) visualised behind and above well-fi lled uri-
nary bladder, sitting in front of spine. ( b ) Cystic dysplastic ectopic kidney (+ +) sitting in front of psoas
muscle distally to its normal position, only seen by meticulous search using graded compression; some
residual parenchyma seen – ureter was draining ectopically into vagina causing constant dribbling
NOTE : Small ectopic kidneys may drain ectopically and can still have function –
this may cause symptoms such as urinary dribbling (when inserting into vagina or
distal to sphincter). If both kidneys not seen in normal position; meticulous search
of entire abdomen mandatory.
330
10 Ultrasound of the Urogenital Tract
Fig. 10.9 Horseshoe kidney. Parenchymal bridge ( callipers ) of a horseshoe kidney depicted in
front of aorta, IVC and vertebral body connecting right and left moiety; mesenteric vessels seen in
front of renal parenchyma in this axial abdominal midline section
Renal Agenesis
Only compatible with extrauterine life only if unilateral – single (hypertrophic) kidney
on other side. Often constitutes end point of disturbed fetal development, e.g. dysplastic
or cystic kidney regressed and cannot be seen any longer. In these children high probability of ipsilateral genital malformation – should be explicitly searched for.
NOTE : Bilateral renal agenesis fatal, usually diagnosed prenatally, leads to severe
hypoplasia of lung.
Fusion Anomalies and Other Rare Findings
Horseshoe kidney – most common anomaly: lower poles attached at midline, form
parenchymal bridge in front of aorta (Fig. 10.9 ); associated with impairment of
urinary drainage, higher risk for being injured in abdominal trauma.
Cross - fused dystopia , triple kidney and other rare variations – not addressed in detail.
Bladder anomalies – such as duplex bladder rare; bladder exstrophy not target of
US investigations (only for assessing kidneys).
10.3 Pathology of the Kidney
10.3.1 Congenital Conditions
10.3.1.1 Dysplasia/Hypoplasia
Defi nition
Structural alteration of renal tissue with more or less impaired function; may be
focal or diffuse, unilateral or bilateral; often associated with severe obstructive
uropathy and/or VUR; congenital/inherited or syndromic.
US Findings
Commonly increased parenchymal echogenicity with reduced cortico-medullary
differentiation, potentially with cysts (Fig. 10.10 ) – see also cystic kidney disease
(below) May be smaller.
10.3 Pathology of the Kidney
abc
Fig. 10.10 Hypodysplastic and cystic kidney disease. ( a ) Small, relatively normal looking
kidney (+ +) in a child with end-stage renal failure due to bilateral renal hypodysplasia. ( b )
Dysplastic kidney with completely disrupted parenchymal structure (similar as in ARPKD
(“pepper and salt” appearence)). ( c ) Echogenic widened cortical parenchyma with cortical cyst
in another cystic-dysplastic malfunctioning neonatal kidney in systemic-syndromatous
disease
331
Fig. 10.11 Cystic kidneys: dysplastic cyst, multicystic dysplastic kidney (MCDK). ( a ) Typical
MCDK with large, not connected, peripheral cysts; some central echogenic dysplastic residual
parenchyma. ( b ) Severe fetal obstructive uropathy with multiple cortical cysts and dysplastic
parenchyma in a neonate
a
b
CDS :
Potential cortical vascular rarefaction with increased resistance (RI ↑), depending
on functional impairment; also pseudonormal fl ow patterns with reduced systolic
velocity.
10.3.1.2 Cystic Renal Disease
Defi nition
Often inherited, genetic, congenital condition – even if cysts only manifest later in life.
However, secondary and acquired cystic disease exists, as well as cystic tumours.
US Findings
Usually anechoic structures with dorsal amplifi cation (Fig. 10.11 ). Depending on
size, content and border, classifi ed into various degrees of complexity (adapted from
the Bosniak CT Classifi cation, though without having enhacement pattern available
on US: from grade I = uncomplicated simple cyst to grade IV being a severely complicated, highly suspicious cyst).
332
10 Ultrasound of the Urogenital Tract
Table 10.2 Schematic drawing for DDx of renal cystic conditions Adapted from Riccabona et al.
(2012) Pediatr Radiol:42. Schematic drawing illustrating typical appearance of different renal cystic diseases and conditions
Classifi cation of cysts – see Table 10.2 :
• Simple cyst: (isolated/single) uncomplicated cyst (no content/completely
anechoic, smooth margin, thin wall, no solid component, etc.), localised, with or
without growth. Rarely seen in neonates and infants.
• Multiple cysts: often associated with parenchymal dysplasia or genetic/inherited
cystic kidney disease.
• Complicated cyst(s): as anywhere else – internal echoes and sedimentation, septae, thick wall, irregular border, solid/nodular components, conglomerates of
cysts, large, irregular shape; vascularised compartments best seen by aCDS .
These need follow-up/diagnostic workup, sometimes additional imaging.
Inherited/Congenital Cystic Disease
Often part of ciliopathy complex (autosomal dominant and recessive cystic kidney
disease – ARPKD and ADPKD; glomerulocystic and medullary cystic kidney disease – GCKD and MCKD; and nephronophthisis/tuberous sclerosis complex)
(Table 10.2 ):
• ARPKD : enlarged hyperechoic kidneys bilaterally, with disrupted echotexture
and potential regional echogenicities (“salt and pepper appearance”) due to
microcysts (too small to be resolved by US), with or without some dilatation of
10.3 Pathology of the Kidney
a
bc
d
Fig. 10.12 Hereditary/genetic cystic renal disease: ARPKD, ADPKD, nephronophthisis.
( a ) ARPKD – bilaterally enlarged kidney, in neonates microcysts often not visible by US, some
patchy “pepper and salt” appearances of hyperechoic parenchyma. ( b ) ADPKD – bilateral (groups
of) single cysts of different size (child with known familiar cystic kidney disease). ( c ) Syndromatous
cystic renal disease – unspecifi c cysts in both kidneys in a neonate. ( d ) Nephronophthisis – girl
with end-stage renal failure due to nephronophthisis. Observe the typical parenchymal, radialgrouped cysts seen in late stage of disease
333
collecting system. Often associated with liver fi brosis (maybe initial manifestation of disease) (Fig. 10.12 ).
• ADPKD : larger parenchymal cysts, can be conglomerated or isolated, single or
multiple (associated with cysts in other parenchymal organs, vascular problems
such as aneurysms); need comprehensive follow-up including all respective
changes (Fig. 10.12 ).
• Syndromic cystic kidney disease : many syndromes exhibit renal cysts. Some also
carry increased risk for nephroblastomatosis/malignant degeneration.
Non-genetic congenital cystic disease : often associated with urinary tract obstruc-
tion or high-grade VUR (see dysplasia), rarely familial.
• Multicystic dysplastic kidney (MCDK) : most common entity (see Fig. 10.11 ).
Said to originate from severe early upper tract obstruction causing severe cystic
dysplasia. Caused by impaired connection between ureteric bud and renal blastema. Classically defi ned by multiple large cysts with potentially some echogenic undifferentiated central parenchyma (may even exhibit residual
vascularisation). Continuous transition to severe obstructive uropathy with dysplastic cysts of parenchyma – thus some residual central collecting system or
residual ureter may be visible. Commonly tend to shrink/vanish spontaneously;
however, some may grow, get infected, cause hypertension or undergo tumourous transformation (particularly those with vascularised residual parenchyma).
US monitoring recommended.
334
ab c
Fig. 10.13 Acquired cystic kidney disease and DD. ( a ) Postinfectious cyst: somewhat irregular
cyst at previous site of an abscess. ( b ) Huge cystic mass connected with upper calyx and showing
contrast extravasation on dynamic MRU, consistent with a urinoma or a huge caliceal diverticulum. ( c ) After heminephrectomy a growing liquid formation (
consistent with a postoperative urinoma
10 Ultrasound of the Urogenital Tract
+ ….+) observed at resection site –
1
NOTE : Often associated with ipsilateral genital malformations, similarly to solitary
kidneys, where contralateral kidney may have involuted during embryology secondary
to similar phenomena. Cystic renal buds may be found in ectopic position with some
residual or absent function. Thus always carefully assess entire abdomen and genital
tract as well as contralateral kidney, which will develop compensatory hypertrophy.
Acquired Cystic Kidney Disease
Defi nition
Number of etiologies occur and exhibit different features: posttraumatic cysts, postoperative cysts, acquired cystic kidney disease in renal failure and after transplantation.
NOTE : Simple renal cyst much rarer in childhood than in adults – every cyst
detected in an infant and young child requires detailed assessment + follow-up.
DDx
Caliceal diverticulum, tertiary calix, cystic remnants of abscess/infection/trauma,
urinoma, and cystic tumours (Fig.
10.13 ).
Role of US
Ideal method for initial investigation/follow-up.
NOTE : Number of cysts and appearance of parenchyma do not necessarily correlate with renal function.
Additional Imaging
Depending on underlying entity – sometimes no additional imaging, sometimes
assessment for VUR (VCUG/ce-VUS), renal function (scintigraphy/MR urography) or ectopic renal remnants (scintigraphy/MR).
Rarely – if unclear or suspicious for malignancy – DDx by MR (CT if MR
unavailable).
10.3.1.3 Alteration of Urinary Drainage
Various underlying entities that cause pathologically altered urine fl ow/drainage.
Often manifests fetally by “hydronephrosis” (HN).
Obstructive and refl uxive entities need to be differentiated without specfi c
features.
Consider alternate dysplastic dilated system/ureter without impairment of
urinary drainage.
10.3 Pathology of the Kidney
Table 10.3 HN grading in neonates and infants – according to ESPR and ESUR recommendation
Pediatr Radiol (2008):38. HN 0 = no collecting system or minimal renal pelvis visible, considered
normal. HN I = just renal pelvis visible, axial diameter <7 mm, usually considered normal. No
calices visible. HN II = axial renal pelvis diameter 7–10 mm; some calices visible, with normal
shape and contour. HN III = marked dilatation of renal calices and pelvis >10 mm, fl attened papilla,
rounded fornices, no parenchymal narrowing. HN IV = gross dilatation of entire collecting system
with narrowed parenchyma. HN V = used sometimes to communicate an extreme HN IV with only
thin, membrane-like residual parenchymal rim. The classifi cation was developed trying to integrate the Hofmann US grading and the SFU classifi cation (Fernbach et al.) for US grading of
(congenital) “hydronephrosis”. NOTE: As this is specifi cally adapted to needs in early childhood,
this classifi cation differs from the common adult grading US grading and can be less useful in
older children, in acute obstruction without underlying dilating uropathy, in dysplasia and as soon
as there is scaring or clubbing
335
Hydronephrosis (HN)
Defi nition
Term originally used to describe any dilatation of collecting system.
Today, due to improved resolution of US equipment, normal distension of pelicaliceal system visualised even fetally – thus HN does not defi nitely indicate
pathology.
Standardised HN grading established, adapted from Society of Fetal Urology
(SFU) Classifi cation and Hoffman’s paediatric US HN grading system (HN 0° –
IV°, see Table 10.3 ). Defi nition relies not on millimetre of pelvic width but visibility
and confi guration of collecting system and thinning of parenchyma. Grading independent of aetiology.
Additional US signs that may indicate pathology and prompt further workup
(“extended criteria”): thickening of ureteral/pelvic wall (>1 mm, nonspecifi c – seen
in infection, oedema, obstruction, VUR), renal parenchymal pathology (e.g. cysts,
altered cortico-medullary differentiation, and altered echogenicity), renal size alterations, dilatation of ureter, and bladder pathology.
Ureteropelvic Junction Obstruction (UPJO)
Defi nition
Narrowing/stenosis of ureteropelvic junction causing impairment/obstruction of
urinary drainage. Aetiology usually congenital, may be acquired. Commonly associated with signifi cant prenatal HN (≥II°).
NOTE : Dilatation best assessed after end of fi rst postnatal week – as physiological
renal immaturity prevents fi lling of collapsed dilated system during fi rst days of life.
Standardised hydration essential for proper recognition and grading, particularly for
follow-up investigations.
336
10 Ultrasound of the Urogenital Tract
US Findings
Dilatation of pelvi-caliceal system (HN grade III°–V°) – lower grades usually associated with non-obstructive UPJA or lower grade VUR without thinning of parenchyma and preserved cortico-medullary differentiation. Ureropelvic junction
narrowed/not depictable; proximal ureter very narrow:
• Pelvic ectasia: only pelvis dilated, calices visualised, but normal confi guration,
sometimes associated with non-obstructed ureteropelvic junction anomaly (UPJA).
• HN IV° (and V°) usually indicates high-grade UPJO (Fig. 10.14 ).
• Signs for (chronically) decompensated obstruction: severe thinning of paren-
chyma, decreased parenchymal echogenicity, lack of cortico-medullary differen-
tiation, and delayed or missing normalisation under diuretic stress by furosemide
(diuretic urosonography). Potentially dysplastic cysts.
NOTE : Dilatation does not equal obstruction – US cannot diagnose obstruction. Even
severe obstruction may show only minor distension under insuffi cient hydration/
decreased function or with intermittent as well as per acute obstruction (e.g. urolithiasis). Diagnosis of severe/decompensated obstruction (which needs treatment to prevent
deterioration of renal function/growth potential) relays on functional imaging.
CDS
Look for accessory/additional renal vessels that may impair ureteropelvic junction (Fig. 10.14 ):
• In chronic and non-obstructive dilatation RI symmetric.
• In acute obstruction asymmetric elevation of RI in affected kidney.
• Also assess potential rarefaction of peripheral vascularity (sign of chronic decom-
pensation with already reduced renal function/scarring), best visualised on aCDS.
Postoperative transient thickening of pelvic wall, pelvis often smaller (as reduced by
surgery) and dilatation of calices often persists for long time – only normalises over
years, potentially focal perfusion impairment/scar (e.g. at site of perioperative drain).
NOTE : For assessing split renal volume, the dilated collecting system has to be
subtracted – best using 3DUS (allows segmentation of collecting system that can be
deducted from overall renal volume, thus allowing exact parenchymal volume calculation – see Figs. 1.30 and 1.31 ). Can then be compared to non-obstructed contra-
lateral side (= split/relative renal size).
Additional Investigations
MAG3 scintigraphy: gold standard for assessing renal function/urinary drainage.
IVU: outdated – replaced by MRU, indicated in complex anatomy, particularly
preoperatively
• In some situations – particularly postoperatively – modifi ed focused IVU helpful
by assessing anatomy/obstruction (only need few well-timed focused images).
Dynamic diuretic MRU: will in future allow for additional functional assessment.
• No indication for CT, even accessory renal artery seen by US/CDS and early
angiographic phase of MRU.
VCUG or ce-VUS: VUR assessment – particularly if indirect signs seen on US.
• Postoperatively some perform fl uoroscopic assessment of drainage before
removing drain.