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316
9 US of the Gastrointestinal (GI) Tract
a
b
c
Fig. 9.25 Crohn’s disease. ( a ) Thickened wall (+ +) with stenotic bowel lumen, some preserved
wall stratifi cation, lack of compressibility, echogenic mesenteric reaction and in patient with acute
Crohn’s disease . ( b ) Cross section through terminal ileum with thick wall, narrow lumen and echo-
genic mesenteric reaction. ( c ) Extended view of Crohn’s disease helps to better visualise and measure
the entire extent in long affected segments. Again note reactively involved echogenic mesentery
• Ulcerating colitis (most important differential diagnosis) only effects colon (see
below).
US Finding
• Thickening of bowel wall with intramural lymph nodes, reactive echogenic/
enlarged/stiff mesentery (may exhibit comb sign created by multiple vessels),
commonly many enlarged lymph nodes (Fig. 9.25 ).
• Affected bowel segments incompressible/stenotic.
• Often seen in terminal ileum (+ appendix), all other segments may be involved.
• Secondary affected bowel loops may form infl ammatory pseudotumorous
conglomeration.
• In chronic stages – residual stenosis, some residual thickening, signs of ileus,
fi stulae tracts and abscess formation.
CDS
• Impressive hypervascularity and hyperperfusion on spectral analysis (high diastolic fl ow, low RI) of bowel wall in active stages (Fig. 9.26 ).
• Used to judge activity:
– Higher resistance fl ow pattern with lower fl ow velocities indicate either
beginning necrosis or improvement under therapy, even if wall remains thick;
stenosis may persist.
– Chronic stages – no hypervascularisation. No hyperaemia.
Role of US
• Essential part of initial work-up/initial diagnosis, but also for follow-up.
• By fi lling bowel with saline enema or drinking formula (similar to those used for
MR-enteroclysis), bowel can be distended and stenotic components can be
observed on US; even fi stula may sometimes be visualised (Fig.
9.27 ).
9.2 Bowel
317
ab
Fig. 9.26 CDS in Crohn’s disease. ( a ) aCDS superbly visualises hypervascularity of bowel wall
in acute Crohn’s disease. ( b ) CDS with spectral trace proves vascular nature of colour signals,
demonstrates low-resistance hyperaemic fl ow in acute phase
ab
Fig. 9.27 Complications in Crohn’s disease: fi stula, stenosis. ( a ) Regional stenosis in acute
Crohn’s disease with thickened bowel wall (+ +) and lack of intraluminal air (which can still be
appreciated as echogenic band before and after stenosis) at most severe narrowing of bowel lumen.
( b ) Fistula tract with air bubbles ( arrow ) indicating connection from bowel lumen to abscess pocket
Complementary Imaging
• MR-enteroclysis, colonoscopy.
• CT enteroclysis reluctantly used in children due to radiation issues, particularly
as repeated follow-up exams would lead to unacceptably high cumulative dose.
• Fluoroscopic enteroclysis only used in selected few cases.
• Plain fi lm valuable in case of suspected perforation.
9.2.6.6 Colitis
Autoimmune condition, bacterial/viral, toxic or antibiotic induced, neutropenia
(after chemotherapy) or granulomatous disease – all may manifest during childhood.
Ulcerative colitis only effects colon/sigmoid, can be multi-segmental:
• DDx for Crohn’s disease: histology after colonoscopy, no small bowel involved,
slightly different US appearance (ulcers seen).
US Finding
• Thickening of colon wall, potential intramural lymph nodes, reactive echogenic/
enlarged/stiff mesentery, enlarged lymph nodes possible as well as some ascites.
318
9 US of the Gastrointestinal (GI) Tract
Fig. 9.28 Colitis. Enlarged lax left colon segment with complex atypical content and slightly
thickened wall without wall destruction, less compressible. No ulcerations seen (Clostridium
colitis)
• Disruption of inner mucosal layer by ulcerations.
• Affected segments painful and less compressible or dilated, with atypical content
(Fig. 9.28 ).
NOTE : Usually thickening less extensive than in Crohn’s; appearance may vary
with underlying entity.
• In chronic stages – residual stenosis, some residual thickening, fi stula tracts/
abscess formation rare.
CDS
• Hypervascularity/hyperperfusion (on spectral analysis – high diastolic fl ow, low
RI) of bowel wall.
• Chronic stages – no hypervascularisation.
Role of US
• Essential part of initial diagnosis, but also for follow-up.
• Filling colon with saline enema (“sonographic hydrocolon”): better distension,
improved view, polyps and stenotic components better assessable.
Complementary Imaging
MR-enteroclysis, colonoscopy.
9.2.6.7 Other Inflammatory Bowel Conditions
Maldigestion and malabsorption syndromes, etc. may lead to infl ammatory reaction
of bowel (e.g. coeliac disease, various food intolerances, granulomatous disease/
sarcoidosis).
Bowel may also be affected in many other conditions: Kawasaki disease, cystic
fi brosis, lymphangioectasia (“protein loosing enteropathy” – to be differentiated
from partial chronic volvulus in malrotation), chronic congestive situations (portal
hypertension), graft versus host disease, during/after chemotherapy, etc.
In chronic stages atrophy of affected bowel segments (mostly mucosa), rarefac-
tion of folds, etc occur.
US Finding
• Mostly/initially nonspecifi c fi ndings – as in gastroenteritis: thickening of bowel
wall (particularly mucosa), increasingly hazy differentiation of wall layers due to
oedematous changes, atypical content.
9.2 Bowel
319
ab
Fig. 9.29 Bowel trauma. ( a ) Subacute impressive bowel wall haematoma after vehicle accident.
CDS activated to document avascular nature of pseudotumorous lesion. ( b ) Complex free fl uid
behind and above bladder in subacute posttraumatic haemoperitoneum. Note sedimentations
• In chronic/later stage: wall narrowing, mucosa becomes atrophic, stratifi cation
of bowel wall may be lost and folds rarefacted/small.
• Reactive lymph nodes may appear, altered peristalsis often observed (transient
ileo-ileal intussusception), atypical content of bowel lumen.
• Secondary ascites, pleural/pericardial effusion, hepatopathy, etc. may be noted.
Role of US
Never diagnostic – but US may give diagnostically valuable information in unclear
abdominal situations, identifying involvement of bowel in present condition – thus
directing further work up.
9.2.6.8 Bowel Trauma
Haematoma or perforation/rupture, as well as vascular/perfusion insult.
US Finding
• Most often seen in duodenum, or fl ank area.
• Regional thickening of bowel wall (oedema, haematoma) with atypical appearance which changes over time, from inhomogenously hyperechoic to eventually
complex hypoechoic (Fig. 9.29a ).
• Reactive changes of mesentery, reactive enlarged lymph nodes in later stage.
• Complex ascites, particularly if ruptured (Fig. 9.29b ).
• Free peritoneal air (see Figs. 8.23 and 8.24 ). Secondary stenosis.
CDS
• May show reactive hypervascularity and hyperperfusion or even necrotic nonperfused sections in vascular injury.
Role of US
US may depict indirect fi ndings (perfusion disturbance, free air, thickened wall,
disruption site, haematoma ...) – not very good in ruling out any condition, particularly in early stage.
Ultrasound of the Urogenital Tract
10
Michael Riccabona
Contents
10.1 Requisites ..................................................................................................................... 322
10.1.1 Indications ...................................................................................................... 322
10.1.2 Preparation ..................................................................................................... 322
10.1.3 Transducers .................................................................................................... 322
10.1.4 Positioning ..................................................................................................... 323
10.1.5 How to Investigate.......................................................................................... 323
10.2 Normal Findings .......................................................................................................... 324
10.2.1 Bladder ........................................................................................................... 324
10.2.2 Kidney ............................................................................................................ 325
10.3 Pathology of the Kidney ............................................................................................... 330
10.3.1 Congenital Conditions ................................................................................... 330
10.3.2 Infl ammatory Renal Parenchymal Conditions ............................................... 344
10.3.3 Vascular Conditions ....................................................................................... 348
10.3.4 Nephrocalcinosis ............................................................................................ 352
10.3.5 Urolithiasis ..................................................................................................... 353
10.3.6 Other Important Renal Parenchymal Disease ................................................ 354
10.3.7 Renal Failure (RF) ......................................................................................... 355
10.3.8 Renal/Urinary Tract Trauma .......................................................................... 355
10.3.9 Renal Tumours ............................................................................................... 357
10.4 Renal Biopsy and Interventions ................................................................................... 359
10.4.1 Renal Biopsy .................................................................................................. 359
10.4.2 Drainage/Nephrostomy .................................................................................. 360
10.4.3 Postoperative Imaging .................................................................................... 361
10.5 Renal Transplant .......................................................................................................... 363
10.5.1 Normal US Findings in Renal Transplant ...................................................... 363
10.5.2 Pathologic US Findings ................................................................................. 364
M. Riccabona
Division of Pediatric Radiology, Department of Radiology,
University Hospital Graz, Auenbruggerplatz 34,
Graz 8036, Austria
e-mail: michael.riccabona@klinikum-graz.at
M. Riccabona, Pediatric Ultrasound,
DOI 10.1007/978-3-642-39156-9_10, © Springer Berlin Heidelberg 2014
321
322
10.6 Adrenal Glands and Pararenal Space ........................................................................... 365
10.6.1 General Remarks ............................................................................................ 365
10.6.2 Typical Normal US Finding ........................................................................... 365
10.6.3 Pathologic Findings ........................................................................................ 366
10.7 US of Urinary Bladder ................................................................................................. 370
10.7.1 Requisites ....................................................................................................... 370
10.7.2 Pathologic Findings ........................................................................................ 371
10.7.3 Paravesical Changes ....................................................................................... 376
10.7.4 Role of US ...................................................................................................... 377
10.8 US of Male Genitals ..................................................................................................... 377
10.8.1 US Technique ................................................................................................. 377
10.8.2 Normal Findings ............................................................................................ 378
10.8.3 Common Pathologic Findings ........................................................................ 378
10.8.4 Infl ammation – Orchitis, Ependymitis ........................................................... 381
10.8.5 Scrotal Trauma ............................................................................................... 383
10.8.6 Torsion ........................................................................................................... 383
10.8.7 Testicular Tumours ......................................................................................... 384
10.8.8 Role of US and Additional Imaging .............................................................. 385
10.9 Female Genitals ............................................................................................................ 385
10.9.1 Indications ...................................................................................................... 385
10.9.2 Requisites ....................................................................................................... 386
10.9.3 Transducers .................................................................................................... 386
10.9.4 How to Perform Investigation ........................................................................ 386
10.9.5 Normal Findings ............................................................................................ 386
10.9.6 Pathologic Findings ........................................................................................ 388
10 Ultrasound of the Urogenital Tract
10.1 Requisites
10.1.1 Indications
(Fetal) hydronephrosis (HN), urinary tract infection (UTI), haematuria, failure to
threive, suspicion of VUR, obstructive uropathy, renal failure, enuresis, micturition
problems, urolithiasis, involvement in systemic or syndromic disease, high blood
pressure, caliceal malformation, trauma, tumour, nephritic and nephrotic syndrome,
renal transplantation, pre-/postoperatively, etc.
10.1.2 Preparation
Good (physiologic) hydration, suffi ciently fi lled bladder.
10.1.3 Transducers
Commonly (micro-)curved arrays with age-adapted frequency:
• Additionally linear transducer, particularly for neonates and infants, detailed
analysis of renal parenchyma, perineal access, scrotum/penis/inguinal area.
• For deep vessels and initial overview, sector transducers can be used.
10.1 Requisites
323
10.1.4 Positioning
Usually supine and fl ank and ventral access (also for perineal US), additionally
prone with dorsal transducer position (paravertebral).
10.1.5 How to Investigate
Always begin with bladder in longitudinal and axial sections:
• Include oblique section through ostia and distal ureters.
• Observe bladder neck.
• Bladder wall (thickness, confi guration, trabeculation?), potential urachus remnants.
• Assess perivesicular space, potentially include perineal US (for urethra, best
during voiding).
• Post-void assessment (bladder/residual volume: use equation L × W × H × correc-
tion factor (Fig. 10.1 ), correction factor varies based on shape of bladder –
spheric confi guration = 0.5, rectangular confi guration = 1.0).
Assess both kidneys from ventral, lateral and dorsal in longitudinal and cross
sections:
• Evaluate entire organ; document any abnormalities in two planes.
• Assess: shape, size, position, contour, parenchymal echogenicity and corticomedullary differentiation, collecting system dilatation (if enlarged, measured in
axial plane) and thickening of pelvic wall and peripelvic fat/fi brotic tissue.
• Calculate renal volume ( L × W × H × 0.53).
• Assess vascular anatomy (CDS) (e.g. accessory renal artery); follow vessels to
origin or drainage (e.g. retro-aortal left renal vein). Add spectral analysis if
indicated from main as well as intrarenal vessels (from upper, middle and
lower segment).
• aCDS is applied for peripheral vasculature (e.g. focal perfusion defects?).
NOTE : Physiologic difference in colour intensity between highly vascularised cortex
and less vascularised medullae. Compare both sides in relation to perirenal structures.
• Always assess perirenal space (adrenal gland).
• Try to assess pelvi-ureteric junction (open? obstructed by vessel? kinking?...);
follow ureter downwards, if dilated.
• Assess collecting system after voiding (changes in dilatation?).
CDS : Document ureteric jet into bladder (symmetric? position of ostium?), vascular
anatomy extrarenally as well as main intrarenal arteries (proper scale setting not to
miss aliasing and turbulences at sites of possible stenosis or AVF...). Assess for possible twinkling (calcifi cations and sedimentations).
10.1.5.1 Diuretic US
Used for assessment in hydronephrotic kidneys: standardised diuretic stress induced
by medication (e.g. furosemide, dose = 1 mg/kg, up to 20 mg) given orally or IV
(acts faster). Repeat assessment of kidney till fi ndings (dilatation of collecting system, Doppler fl ow spectra) have returned to baseline – delayed or missing normalisation of fl ow patterns after diuretic stress indicates signifi cant obstruction.
324
a
DD
W
10 Ultrasound of the Urogenital Tract
b
e
Fig. 10.1 Normal bladder US. ( a ) Schematic drawing with respective images demonstrating
standard measurements for volume calculation. Correction factor varies with bladder shape.
Additionally bladder wall thickness may be an indicator for bladder pathology (>2 mm in full,
>4 mm in empty bladder), L length, W width, D depth. ( b ) Longitudinal (extended view technique
is helpful in large-size bladders for proper measurement); ( c , d ) axial section – with axial measure-
ments ( callipers ) for volume assessment; calculation depends on bladder shape that defi nes the
correct correction factor: in sphaeric-ellipsoid shape factor = 0.5 ( c ), in a rectangular shape it is 1
( d ). Note additionally thickened and trabeculated bladder wall. ( e , f ) Open bladder neck in axial
( e ) and sagittal ( f ) view – a potential sign for bladder instability or other functional disturbance. ( g )
Ureteric infl ow jet – best seen on CDS: note the asymmetry in this example
f
c
d
g
10.2 Normal Findings
10.2.1 Bladder
Well-fi lled bladder has smooth contour and muscular wall, not >2–4 mm thick
(depends less on age than on fi lling):
• Ostium at latero-cranial end of bladder trigone as well as distal ureters often seen
physiologically in well-fi lled bladder and good-hydrated children.
• Assess bladder volume (see above and Fig. 10.1 ). Simple equation often used to
defi ne normal range: volume (ml) = [age (in years) + 2] × 30.
10.2 Normal Findin gs
abc
Fig. 10.2 Normal neonatal kidney. ( a ) Longitudinal section of right neonatal kidney with length
measurement (+ ....+). Note physiologically relatively high echogenicity of cortex (similar to
liver), pronounced cortico-medullary differentiation and some (transient) echogenicity in distal
medulla. ( b ) Axial section of left kidney with measurements ( callipers ) – same appearance of
parenchyma as in ( a ). ( c ) Axial section, neonatal left kidney: same parenchymal appearance as in
( a , b ) but some widening of renal pelvis (<5 mm) with some slight prominence of the pelvic wall
(<1 mm) – this may be normal, but may rectify a follow-up study
325
• Bladder neck closed unless there’s an urge to void; after voiding bladder neck
should be closed. Open bladder neck, thickened bladder wall, irregular inner
contour with trabeculation and pseudo-diverticulae, high bladder tension or
atypical contour may raise suspicion of neurogenic bladder/functional
disturbance.
• For assessing retrovesical structures (distal ureter, retrovesical space, internal
genitalia, etc.), adequate manipulation of TGC adaptation necessary. Use ureteric jet for defi ning ostium position and assessing symmetry of urine infl ow.
NOTE : Nodular wall component at bladder roof may be physiologic as remnant of
urachus. Furthermore in neonates the urachus may still be depicted for a couple of
weeks but without patent lumen. In neonates with still immature bladder function,
some residual urine does not indicate pathology.
10.2.2 Kidney
Parenchymal appearance changes with age:
• Neonatally – relatively thick parenchyma with accentuated cortico-medullary
differentiation and rather echogenic cortex (may be more echogenic than adjacent liver tissue), with hypoechoic medullae. Distal medullae and papillae may
exhibit echogenicities (transient physiologic phenomenon that resolves spontaneously) (Fig. 10.2 ). With age, cortico-medullary differentiation gets less pro-
nounced; echogenicity of cortex decreases. Echogenicity of distal medulla
becomes homogeneously hypoechoic (Fig. 10.3 ).
• Sometimes papilla and pelvic wall become more echogenic with some slight
echogenicity around central structures due to peripelvic fat and fi brosis.
• Calices and renal pelvis may be visible, particularly with modern high-resolution
transducers, without indicating urinary transport alteration (Fig. 10.4 ).
326
abc
Fig. 10.3 Normal kidney in childhood. ( a ) Longitudinal kidney scan (from dorsal) with length
measurement. ( b ) Axial scan of right kidney through liver with measurement of diameter.
( c ) Depictable extrarenal pelvis and proximal ureter (+ +), may be normal in a well-hydrated child
10 Ultrasound of the Urogenital Tract
ab
Fig. 10.4 (Normal) collecting system in neonates and infants. ( a , b ) Normal neonatal kidney,
despite (physiologically) prominent cortico-medullary differentiation and some dilatation of the
collecting system – but with normal confi guration of fornices and papillae (HNII)
• Assess fornices and papilla to demonstrate normal shape; assess renal pelvis
wall (should not be thickened). In the hilum, the renal vein and artery are to be
recognised and can be differentiated by following these structures to their vascular origin, whereas the pelvis curses downwards towards ureteropelvic
junction.
• Renal size: standardised measurements and volume calculation; compare with
age-/weight-adapted growth charts (Table 10.1 ). Always compare to other side
(calculate relative renal volume: volume right + left = 100 %). If different/one
kidney enlarged or smaller, always meticulously try to assess potential
reasons.
CDS : After fi nding vessels, identify them by fl ow direction; perform spectral analy-
sis from duplex trace. Slightly higher arterial RI (0.75–0.80) physiologic in neonates, then quickly maturing to normal adult values (RI ~ 0.67 ± 0.03) (Fig. 10.5 ).
Also observe shape, particularly of systolic infl ow – fl attened and slow acceleration
of systolic upstroke typical for renal artery stenosis.