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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
Fig. 15.33 Urinary tract trauma. (a) Blood sedimentation in urinary bladder after renal trauma.
(b) Perirenal clear uid—consistent with posttraumatic urinoma. (c, d) Focal altered contour and
structure of kidney (c) after trauma—only aCDS (d) clearly demarks extent of renal injury. (e)
Relatively normal appearance of kidney, but no perfusion on aCDS (colour box)—indicating
devascularisation due to hilar vascular injury of the kidney
421
• Rarely catheter angiography (potential recanalisation of renal vessels in central
vessel compromise).
• Follow-up by US, DMSA scintigraphy, MRI.
15.3.9 Renal Tumours
15.3.9.1 Benign Tumours
Mostly hamartoma, angioma, angiomyolipoma (tuberous sclerosis), and rarely
adenoma.
15.3.9.2 Pre- or Semi-Malignant Tumours
Nephroblastomatosis (remnants of metanephrogenic tissue, may develop into Wilms’
tumour), neonatal mesoblastic nephroma (mostly benign, rare malignant entities).
15.3.9.3 Malignant Tumours
Most commonly Wilms’ tumour (nephroblastoma), rhabdoid tumour, renal sarcoma, renal cell carcinoma—other entities rare.
US Findings (Fig.15.34)
• Angiomyolipoma exhibits more or less typical echogenic tissue structure.
• Cystic nephroma appears as multicystic mass that may manifest segmentally
with tumourous enlargement, disruption of normal echogenicity, small septae,
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M. Riccabona
Fig. 15.34 Renal tumours. (a) Focal echogenic renal tumour, typical for an angiomyolipoma. (b,
c) Focal renal tumour of similar echogenicity as renal cortex on gray scale (b), better visible by its
exophytic behaviour and its (hyper)vascularity on CDS (c), in a patient with tuberous sclerosis—
consistent with an atypical angiomyolipoma—needs follow-up and sectional imaging. (d)
Nephroblastomatosis: multiple peripheral renal tumourous nodules, partially difcult to appreciate
on gray scale, better outlined by aCDS. (e) Typical appearance of Wilms tumour: large mass with
relatively homogenous tissue and cortex-like echogenicity. (f, g) More and less cystic Wilms
tumours. (h) 3DUS in an echogenic Wilms tumour, helpful for more accurate tumour volume calculation; the right lower box shows a 2DUS image of the same patient with an additional exophytic
nephroblastomatotic focus in the upper pole (
+…+). Note dilatation of collecting system caused
1
by impaired drainage due to compression of the renal pelvis by the large tumour. (i) Focal renal
lesion (
+ …+) in a child with lymphatic leukaemia—consistent with renal involvement. (j)
1
(Congenital) Renal tumour in a neonate with subtotal destruction of the kidney, only leaving a
subtle peripheral rim of original kidney parenchyma—consistent with a mesoblastic nephroma. (k)
Atypical tumour (
+ …+) in an older girl. Most common DDx: rhabdoid Wilms tumour, renal
1
sarcoma, renal cell carcinoma
15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
423
usually with little perfusion. Larger solid areas, nodular wall structure, hyperaemia or large cystic components with haemorrhage may indicate another underlying entity (e.g. cystic Wilms’ tumour).
• Other tumours have nonspecic appearance of any mass lesion—may exhibit
pseudocapsule, growth from kidney, displacing surrounding structures, local
lymph node metastases and—particularly in Wilms’ tumour—relatively often
have vascular invasion with renal vein thrombosis reaching even into IVC and up
to right atrium (may also occur in renal cell carcinoma). Secondary necrotic,
cystic, haemorrhagic changes may be present.
• Assumption of entity depends more on age than on US/imaging ndings.
• Tumours usually large when diagnosed (different for angiomyolipoma/
hamartoma).
DDx
Focal nephroma/inammatory pseudotumour, xanthogranulomatous pyelonephritis, inltration in systemic disease (lymphoma), hypertrophic column of Bertin,
other complex cysts.
Role of US
Initial diagnosis—nd/conrm suspected lesion, dene size (volume calculation)/
relation to central renal structures, surrounding organs/tissue, assess patency of central structures (artery, vein, pelvis), give rst information on stage (inltrating/local/
liver metastases?).
Later-follow-up, assessment of complications.
Additional Investigation
• Sectional imaging by MR (or CT, if MR unavailable) mandatory, particularly in
suspected malignancy—adhere to local tumour imaging protocols.
• Sometimes US-guided biopsy (varies with country/continent).
15.4 Renal Biopsy andInterventions
Also see chapter on interventional US for general recommendations/guidelines.
15.4.1 Renal Biopsy
Biopsy often necessary for histologic assessment of renal parenchymal disease—
biopsy of focal renal lesions far less common than in adults, particularly
in Europe.
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M. Riccabona
Renal biopsy should always be performed under US guidance for reducing
risks:
• Standardised procedure with pre-interventional assessment, time out, periinterventional guidance, postinterventional follow-up.
• Standardised protocols should be used.
• Pre-interventional US performed to assess kidney for potential dilatation, thickness of renal parenchyma, potential biopsy risks (e.g. abnormal vessels or preexisting arteriovenous malformations/stula), and impaired access. At that time
needle length/size dened—depending on the depth of the kidney, size of sample
required, thickness of parenchyma.
• Most commonly 20–18(−16) Gauge needles with 1.2(−2) cm core length advisable, potentially using coaxial technique.
• Use of steering device (biopsy guide) and (semi-)automated biopsy guns
helpful.
• Thereafter validation of indication and coagulation check, informed consent,
time out.
• US-guided biopsy (see also respective chapter on interventional US): performed
in prone position (for native kidneys)—with support under belly to avoid displacement of the lower pole of the left kidney (usually targeted to avoid injury of
adjacent liver on the right side).
– Local and systemic analgesia/sedation may be necessary with adequate
monitoring.
– Biopsy direction—parallel to major segmental vessels branching into periph-
ery; CDS helpful to avoid large vessels.
– Real-time monitoring of needle positioning and biopsy using cine loop
advisable.
• Post-biopsy US: check for potential post-biopsy complications (e.g. bleeding,
haematoma, haematuria, infarction, and AV stula), recommended immediately
afterwards, 3–6h and 24h after intervention. Standardised post-biopsy management helpful (Fig.15.35).
• See also ESPR/ESUR recommendations in Pediatr Radiol (2015).
15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
425
a
bc
de
Fig. 15.35 Renal biopsy. (a) Renal biopsy, dorsal approach to the lower pole of the left kidney:
needle path outlined by dotted lines, needle (echogenic line) already advanced to renal capsule. (b)
Needle now red, position and depth of needle nicely visualised by image from cine-loop documentation. (c) aCDS superiorly helps to depict postinterventional subcapsular haematoma which
in early stages is of similar echogenicity as renal cortex; also observe triangular perfusion defect
in lower pole, indicating regional perfusion defect due to injury of respective vessel causing a
small infarction. (d, e) Postinterventional follow-up (3h after procedure) depicts focal aliasing on
CDS, consistent with an arteriovenous stula; respective ow alterations of feeding artery and
draining vein assessed by spectral analysis (e) conrming shunt ow by demonstrating arterialised
ow pattern in draining vein
15.4.2 Drainage/Nephrostomy
US enables safe access to dilated system or abscess. Steering devices attached to
transducer sometimes helpful; alternatively freehand technique used. Always dene
adequate access that allows for sufcient parenchymal coverage of targeted area to
avoid leakage/urinoma formation.
Access achieved commonly using trocar or Seldinger technique; additional sup-
plementing uoroscopy may be helpful to assess leakage, positioning, and anatomy
after contrast instillation once successful access is gained under US guidance or for
Seldinger technique using guide wires and dilatation of the parenchymal tract.
15.4.3 Postoperative Imaging
To assess postoperative anatomy, to detect complications, and to evaluate success.
For assessment of VUR recurrence or insufcient success of cystoscopic tech-
niques, ce-VUS can be performed as alternative to VCUG even intraoperatively.
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M. Riccabona
15.4.3.1 After VUR Treatment
Cystoscopic Treatment
Injection of material at ostium under cystoscopic guidance.
US can assure patency of ostium by proving ureteric inow jet, may depict
impaired drainage (too large deposits), causing ureteral/pelvicalyceal distension,
potentially associated with stenotic peristalsis of ureter.
Deposits usually seen as echogenic focus in vicinity to transmural distal ureter—
may cause twinkling (Fig.15.36b).
Note Some transient dilatation of ureter normal, may disappear spontaneously;
only if additional new dilatation of pelvicalyceal system noted, obstruction needs to
be considered—then may need further functional assessment/potentially guided
drainage/stenting.
Antireflux Surgery
Different surgical techniques used, ostium appearance varies depending on performed surgery:
• Commonly altered course/potentially altered insertion of ureter visualised.
• Ureter inow jet more difcult to depict.
• Initially ureteric wall thickened/swollen, some ureteral dilatation (Fig.15.36a).
• Only in signicant obstruction higher degree of dilatation of collecting system
observed—some transient mild dilatation often seen in early postoperative phase,
particularly if drains acting as foreign body placed causing reduced ureteral peristalsis.
Note With full bladder there may be kinking of ureter at insertion causing (tran-
sient? intermittent?) obstruction.
Other complications:
• Rarely perivesical haematoma/urinoma—will usually resolve spontaneously
provided sufcient bladder drainage (Fig.15.36e).
• Rarely intervesical clots, commonly catheters (often placed for rst days).
Search for bladder wall injury with urinoma formation, try to localise poten-
Note
tial drains.
Findings in reimplantation for megaureter similar as with antireux surgery—
preexisting dilatation of ureter and wall thickening persist, even in good result with
good function.
15.4.3.2 Findings after Pyeloplasty
Early assessment should focus on depiction of perfusion decits—persisting dilatation normal, does not indicate persisting obstruction:
bc
15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
427
a
de
Fig. 15.36 Postoperative US. (a) Swollen ostium after reimplantation of a megaureter; patency
documented by CDS exhibiting ureteric inow jet. (b) Echogenic deposit at ostium after cystoscopic treatment of VUR (deux instillation). (c) JJ catheter in physiologically stilldilated renal
pelvis after pyeloplasty. (d) Dilated renal collecting system after surgery, with sedimented echoes
in calyx, consistent with postoperative intraluminal blood. (e) Perivesical uid accumulation after
accidental injury to bladder wall in cystoscopic unroong of a huge ureterocele, consistent with a
perivesical urinoma
• Assess position of drain/tip of JJ stent, potentially urinoma/haematoma and postoperative infarctions. Furthermore haematoma/echoes in collecting system
(Fig.15.36c, d).
• Asymmetrically elevated RI/slightly impaired renal perfusion physiologic in
early postoperative setting. Sometimes sectional infarction (vascular damage).
• Perfusion should normalise unless persisting obstruction/chronic damage/scarring is present.
• In early state dilatation often less due to stents or drains—when withdrawn, some
(particularly intrarenal) dilatation persists, degree of extrarenal dilatation
depends on the amount of resected pelvis, does not correlate with potentially
persisting obstruction. Only gradually dilated system will eventually become
narrower over time, renal pelvis usually is immediately smaller due to partial
resection perioperatively—does not indicate absence of obstruction.
• Physiologically some transient increased echogenicity with reduced corticomedullary differentiation (reactive swelling).
• Eventually renal parenchyma normalises—except for those with scarring/persistent damage.
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M. Riccabona
• Renal (parenchymal) growth best monitored using volume calculations—also try
to assess pelvi-ureteric junction, ureteric inow jet into bladder, potentially additional vessels and scarring.
• Additional imaging: MAG3 scintigraphy and/or MR urography, rarely
focused IVU.
Note US poor in assessing/grading drainage—achieved by scintigraphy/MR urog-
raphy; some centres perform pressure tests before withdrawal of postoperative catheter from collecting system under uoroscopic surveillance (pressure point for
contrast drainage into ureter should be <10cm H2O).
15.4.3.3 After Various Interventions
A variety of interventional procedures exist—balloon dilatation, percutaneous
drainage/stenting, endoscopic unroong of ureteroceles, etc.
After Biopsy, Drainage, etc.—See above.
US Findings after Other Interventions
Depend on performed procedure. Used to evaluate/document dilatation of collecting system, potential echoes/structures within system, position of drainages and
stents, assessment of haemorrhage or urinoma and renal perfusion.
After Extracorporeal Lithotripsy (ESWL)
• Assess residual concretions, amount of disintegration, and potential persisting
obstruction (particularly at site of ureteropelvic/uretero-vesical junction) by
residual deposits.
• Tissue damage by shock wave (oedema, haematoma/diffuse swelling/rupture—
either of surrounding tissue and/or kidney).
• Some transient perfusion impairment (reduced peripheral vasculature on
aCDS, elevated RI due to low diastolic flow)—commonly resolves
spontaneously.
15.5 Renal Transplant
US used for pre-, peri-, post-transplant assessment (see also ESPR/ESUR recommendations in Pediatr Radiol 2015):
• Pre-transplant assessment of donor: assess potential preexisting conditions;
insure that living donor left with sufciently functional kidney.
• Recipient evaluation: preexisting renal disease, bladder (capacity/function),
major vessels for planning anastomosis (diameter, patency, course of arteries
and veins).
15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
429
• During transplantation: CDS to assess perfusion of freshly implanted kidney (to
depict early potential compromise of vascular anastomosis allowing for immediate repair).
• After transplantation: repeated follow-up to assess for proper function/potential
complications.
15.5.1 Normal US Findings inRenal Transplant
Commonly large, in the right/left iliac fossa, size/shape depend on donor organ.
Cortico-medullary differentiation often pronounced. CDS exhibits normal vascular
architecture—some transient aliasing at anastomosis during early postoperative
period; use aCDS to demonstrate peripheral normal (perfused) vasculature.
Segmental perfusion defects may correspond to site of biopsy/infarctions (e.g. sacriced accessory/polar arteries). Spectral trace of arterial and venous ow proles
as in normal healthy kidneys (Fig.15.37).
Fig. 15.37 Renal transplant/PTLD. (a) Typical appearance of the parenchyma of a renal trans-
plant, with prominent cortico-medullary differentiation; pelvis visible, also some uid at the upper
pole. (b) aCDS demonstrates normal peripheral vascularity; reduced colour coding of medullae is
physiological. (c) CDS with spectral trace shows altered and reduced arterial peripheral ow and
markedly turbulent and accelerated venous ow due to severe renal swelling—a sensitive, but
nonspecic sign (in this case rejection). (d) Perirenal uid collection—DDx: postoperative urinoma, liqueed haematoma, lymphatic uid collection. (e) Focal complex hypoechoic liquid
lesion adjacent to vascular anastomosis with preserved ow in vessels—seromatous transformation of a perivascular postoperative haematoma (DDx: thrombosed aneurysm). (e) Focal
hypoechoic nodule in transplanted kidney; the child also had similar nodules in original kidney as
well as a group of enlarged mesenteric nodes, consistent with PTLD
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M. Riccabona
Note RI changes nonspecic—depend on number of partially systemic/extrarenal
factors. Persisting singularly renal ndings such as elevated RI (> 80), increased/
fast venous ow, pathologic ow pattern (e.g. delayed systolic upstroke, aliasing/
turbulence), etc. Indicate transplant problems, as well as signicantly decreased
(peripheral) perfusion, particularly on aCDS (e.g. peripheral halo/rim sign).
15.5.2 Pathologic US Findings
Early Post-Transplant Findings (Fig.15.37)
• Perirenal haematoma, cyst formation—may represent lymphocele, urinoma.
• More or less dilatation of collecting system with potentially swelling/thickening
of urothelium.
• Peripheral zones of contusion or infarction (e.g. site of initial biopsy).
• Malposition of drain/catheter—ndings comparable to respective US appearance in native kidney.
• aCDS: assess focal turbulent ow, peripheral minor perfusion, segmental perfusion defects—guide spectral analysis.
• Spectral analysis: impaired diastolic ow, impaired systolic inow, missing/turbulent venous ow—signs for vascular complications.
Note US poor in differentiating between various causes of acute transplant failure
(e.g. acute tubular necrosis, acute ischaemia, renal vein thrombosis, acute rejection).
• DDx narrowed by clinical signs with detailed history of surgery, US features—
eventually may need US-guided biopsy.
Late Post-Transplant Findings
Entities: Lymphocele, infection, cyclosporine toxicity, vasculopathy/stenosis/aneurysm, rejection, urinary obstruction. Most ndings reect respective sonomorphologic features in native kidney.
Rejection: Most sensitive sign—acute enlargement of transplant organ, RI not
specic (tend to be elevated). In suspected rejection only renal biopsy will eventually establish or exclude the diagnosis:
• Some centres perform protocol driven biopsies; others only perform biopsy on
clinical indication.
Helpful to have baseline US in stable uneventful post-transplant period to
Note
allow for comparison during phases with transplant complications. Always include
assessment of potentially remaining native kidneys (e.g. cystic disease,
tumour)+major abdominal structures (e.g. post-transplant lymphoproliferative disease—PTLD, Fig.15.37f) on follow-up US.