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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5790_Библиотеки_им_академика_М_И_Перельмана.pdf
7.5 US in Liver Transplantation
255
7.5.4 Typical Complications
• Vascular: HV occlusion, PV stenosis or thrombosis, HA stenosis or occlusion,
(pseudo-)aneurysm of HA, arteriovenous fi stula and liver infarction
• Collections: Abscess formation, haematoma, biloma and seroma
• Bile complications: bile leakage, bile duct stricture (commonly at site of anastomosis), aerobilia, cholangitis, sludge and stone formation
• Extrahepatic: ascites, splenomegaly, adrenal haemorrhage, pancreatitis, lymphoproliferative disorders, IVC-thrombosis, pleural effusion, etc.
• Parenchymal disease: hypoxia, rejection and lymphoproliferative disorders
NOTE : US nonspecifi c. Diagnosis mostly made on clinical grounds, confi rmed by
biopsy. Because of low sensitivity and specifi city, role of US is to exclude other
graft complications and to detect early potential transplant tumours.
Common US Findings
• Heterogeneity of atypical parenchyma, e.g. in acute rejection or after hypoxia
• Monophasic hepatic vein waveform in all situations with increased liver
resistance
• Increased arterial resistance and pathology of fl ow profi les (stenoses, rejection,
etc.).
Spleen and Pancreas
Michael Riccabona
Contents
8.1 Spleen .............................................................................................................................. 258
8.1.1 Requisites........................................................................................................... 258
8.1.2 Positioning ......................................................................................................... 258
8.1.3 Indications ......................................................................................................... 258
8.1.4 Course of Investigation ...................................................................................... 258
8.1.5 Normal Anatomy ............................................................................................... 259
8.1.6 Normal Variants ................................................................................................. 260
8.1.7 Malformations ................................................................................................... 260
8.1.8 Splenomegaly .................................................................................................... 261
8.1.9 Trauma ............................................................................................................... 261
8.1.10 Splenic Infarction .............................................................................................. 264
8.1.11 Space-Occupying Lesions of the Spleen ........................................................... 265
8.2 Pancreas ........................................................................................................................... 268
8.2.1 Requisites........................................................................................................... 268
8.2.2 Indication ........................................................................................................... 268
8.2.3 Course of Investigation ...................................................................................... 268
8.2.4 Normal Findings ................................................................................................ 269
8.2.5 Variations and Malformations ........................................................................... 270
8.2.6 Infl ammation: Pancreatitis ................................................................................. 270
8.2.7 Trauma ............................................................................................................... 272
8.2.8 Space-Occupying Lesions ................................................................................. 274
8.2.9 Role of US ......................................................................................................... 275
8.2.10 Additional Imaging ............................................................................................ 275
8
M. Riccabona
Division of Pediatric Radiology,
Department of Radiology,
University Hospital Graz, Auenbruggerplatz 3,
Graz 8036, Austria
e-mail: michael.riccabona@klinikum-graz.at
M. Riccabona, Pediatric Ultrasound,
DOI 10.1007/978-3-642-39156-9_8, © Springer Berlin Heidelberg 2014
257
258
8.3 Retroperitoneum, Other Peritoneal and Retroperitoneal Structures,
Abdominal Vessels and Abdominal Wall ........................................................................ 276
8.3.1 Abdominal Vessels ............................................................................................ 276
8.3.2 Vascular Pathology ............................................................................................ 278
8.3.3 Mesentery .......................................................................................................... 281
8.3.4 Mesenteric Lymph Nodes .................................................................................. 283
8.3.5 Free Intraperitoneal Air ..................................................................................... 283
8.3.6 Free Intraperitoneal Fluid: Ascites .................................................................... 285
8.3.7 Retroperitoneal Soft Tissues .............................................................................. 287
8.3.8 Abdominal Wall ................................................................................................. 288
8 Spleen and Pancreas
8.1 Spleen
8.1.1 Requisites
Usually curved linear arrays (and sector transducers) used.
For detailed analysis, linear transducers recommended.
Frequency adapted to age.
8.1.2 Positioning
Supine, prone, lateral decubitus.
NOTE : Due to ribs examination can be unpleasant or tricky, thus cautious transducer
handling necessary.
8.1.3 Indications
• Enlargement of spleen – most common indication for abdominal US in some areas:
– Huge variation in measurements, diffi cult to defi ne standard plane
– High inter-/intra-observer variations – of restricted reliability
• Involvement in systemic disease:
– Enlargement, focal lesions (abscess, fungus, lymphoma, leukaemia)
• Portal hypertension
• Trauma
• Haemolytic anaemia, thrombocytopenia, etc.
• Metabolic diseases, mucopolysaccharidosis, glycogenosis, etc.
• Malformations, syndromes (asplenia, polysplenia, etc.), etc.
8.1.4 Course of Investigation
• Find spleen in intercostal plane in left axillary line, sometimes deep inspiration
or “big belly” helps to visualise entire organ
• Standardised measurements (coronal section with largest diameter/length that
includes the splenic hilar vessels) (see Fig. 1.10 )
8.1 Spleen
Table 8.1 Normal size of spleen depending on age/size and standard measurements
( a ) Graph demonstrating standard measurements plains
( b ) Maximal normal spleen length (mm) in neonates, correlated with body weight (kg)
( c ) Normal spleen volume (ml) during childhood correlated to body height (cm). Volume calcu-
lated by normal ellipsoid equation (correction factor = 0.5, average of depth measurement in two
planes used to reduce errors)
L = length, W = width and D = depth (in mm)
ab
259
Fig. 8.1 Normal spleen. ( a ) Axial view. ( b ) Longitudinal view, with standardised section for
measurement (+ +): adequate section defi ned by hilar vessels, lower pole and upper pole
(medio-posterior)
• Assess entire organ in longitudinal + axial organ sections (see Table 8.1 )
• Always assess adjacent spaces: subphrenic and subsplenic/perisplenic
• CDS helpful when looking for vessel pathology (e.g. posttraumatic aneurysm,
collateral and enlarged veins in portal hypertension, thrombosis/infarction, etc.)
8.1.5 Normal Anatomy
Normal spleen – inverted comma shape, larger surface positioned adjacent to left
diaphragm.
Large parallel vessels seen in hilus – follow into organ and to midline along
pancreas.
Homogeneous organ of rather low echogenicity with smooth margins and
rounded poles (Fig. 8.1 ).
260
ab
Fig. 8.2 Splenunculus/splenule (accessory spleens). Small splenules in two different cases (+ +)
documented in axial ( a ) and longitudinal view ( b )
8 Spleen and Pancreas
Size – see age-adapted normal values (Table 8.1 ), as rule of thumb: maximum
length (cm) = 6 + 1/3 of age (years). Measurements taken in reproducible section
that includes hilar vessels:
• If spleen reaches lower third of normal sized and positioned left kidney =
enlarged
• In neonates shape and position of spleen different (more oblique)
8.1.6 Normal Variants
8.1.6.1 Splenunculus (Accessory Spleen)
Most commonly close to hilus (may be positioned anywhere), usually spheric or
ovoid, same echogenicity as splenic parenchyma, often some connection to spleen
with vascular hilus (arises from splenic vessels) (Fig. 8.2 ).
NOTE : Splenunculi may cause acute abdomen by torsion and infarction, often
notable by lack of CDS signals. Sometimes diffi cult to differentiate from lymph
nodes (or real accessory spleen/polysplenia).
8.1.6.2 Splenic Lobulations and Clefts
Important to avoid confusion with adrenal or renal mass, scars or traumatic lesions.
8.1.7 Malformations
8.1.7.1 Asplenia
Defi nition
No spleen, rare, associated with other systemic malformations and syndromes.
US Finding
No spleen/splenunculus seen.
NOTE : Thorough assess entire abdomen for small/ectopic spleens.
8.1 Spleen
261
8.1.7.2 Polysplenia Syndrome
Defi nition
No normal single spleen, but multiple smaller organs, may be positioned in normal
left upper quadrant or ectopic, often mobile and prone to torsion and infarction.
Rare variant: right-sided position – may be confusing. Shape can vary.
US fi ndings same as in normal spleen.
NOTE : In inverted abdominal or systemic situs, liver is positioned on left side and
spleen in right upper quadrant, often associated with spleen anomalies and variations.
Associated abdominal anomalies: disruption of inferior vena cava, azygos
continuation, pancreas variations, bowel malrotation and renal agenesis/hypoplasia.
Additionally there may be thoracic and cardiac anomalies.
8.1.7.3 Wandering Spleen
Defi nition
Slightly atypical shape, not normally fi xed by gastrosplenic/spleno-renal ligament,
commonly positioned ectopically. Increased risk of torsion and infarction.
US fi ndings same as in normal spleen.
8.1.8 Splenomegaly
Defi nition
Increased size – see normal values.
Caused by infection (acute or chronic, bacterial or viral, other rarer organisms),
congestive in portal hypertension and cardiac insuffi ciency, haemolytic anaemia
and infi ltration/depositions in systemic and metabolic disease (e.g. mucopolysaccharidosis, glycogenosis, leukaemia, lymphoma).
Secondary to (large) cysts and abscesses.
US Findings
Depending on underlying disease, parenchymal structure normal or disrupted. May
be patchy and inhomogeneous.
Echogenicity mostly normal, may be decreased or increased. Sometimes
inhomogeneous.
In signifi cantly enlarged spleens, extended view techniques are helpful to measure
entire length; 3DUS reported to be most accurate for volume assessment (Fig. 8.3 ).
NOTE : In splenomegaly carefully assess for potentially underlying causes (e.g.
liver/portal vein pathology and lymphoma/leukaemia) or additional fi ndings (e.g.,
ascites and gall stone).
8.1.9 Trauma
Defi nition
Spleen injury common in blunt abdominal trauma in children and may lead to acute
haemorrhage.
262
Fig. 8.3 Extended fi eld of
view in splenomegaly.
Signifi cantly enlarged spleen
only measurable using
extended fi eld of view US
Table 8.2 Splenic injury grading system
Grade I
Subcapsular haematoma <10 % of surface area
Capsular laceration <1 cm depth
Grade II
Subcapsular haematoma 10–50 % of surface area
Intraparenchymal haematoma <5 cm in diameter
Laceration 1–3 cm depth not involving trabecular vessels
Grade III
Subcapsular haematoma >50 % of surface area or expanding
Intraparenchymal haematoma >5 cm or expanding
Laceration >3 cm depth or involving trabecular vessels
Ruptured subcapsular or parenchymal haematoma
Grade IV
Laceration involving segmental or hilar vessels with major devascularisation (>25 % of spleen)
Grade V
Shattered spleen
Hilar vascular injury with devascularised spleen
Adapted from American Association for Surgery of Trauma
8 Spleen and Pancreas
Children often compensate even severe haemorrhage for signifi cant time to
eventually deteriorate suddenly, making a thorough US investigation particularly
valuable. Grading is available and should also be attempted when diagnosed by US,
as grade correlates with risk of complications (Table 8.2 ).
US Findings
Potentially increased size due to subcapsular haematoma, which in early
posttraumatic phase sometimes cannot be discriminated from normal spleen tissue;
only perisplenic fl uid or later phases with sedimentation of erythrocytes and
complex fl uid-like appearance of haematoma enables visualisation (Fig. 8.4a, b ).
• aCDS and particularly ce-US improve early detection of splenic injury and
haematoma/acute bleeding (Fig. 8.4c )
• Initially haematoma iso- or hyperechoic to spleen parenchyma, later turning
hypoechoic (Fig. 8.4d )
• Contusions without haemorrhage often only exhibit regionally more
inhomogeneous structure without demarcation of haematoma
8.1 Spleen
263
ab
cd
Fig. 8.4 Spleen hematoma. A series of images demonstrating various appearances of acute splenic
trauma: only slight subcapsular/perisplenic fl uid ( a , b ) with poorly depictable and hazy parenchy-
mal lesion, regional perfusion alteration without depictable parenchymal changes but subcapsular
haemorrhage ( c ) and obvious parenchymal damage ( d )
• In laceration contour disrupted – complex shape, disruption of parenchyma, may
reach central vessels
• Reduced diaphragmatic motion (refl exive-reactive) – helpful indirect sign –
potentially follow-up exam after 6–24 h
Normalisation of tissue will take weeks to months; gradually lesion becomes
increasingly hypoechoic and demarcated/cyst like (Fig.
8.5 ); secondary posttrau-
matic cysts or fi brous scar tissue may remain.
NOTE : Peritoneal fl uid only initially located perisplenic will distribute in entire
abdominal cavity depending on position although originating from spleen – thus
location of intra-abdominal fl uid does not necessarily correlate with origin/site of
injury.
CDS
• Useful to assess vitality or areas with lack of perfusion, e.g. by disruption or
infarction
• In follow-up useful to detect posttraumatic aneurysms or AVF, which may
rupture and cause secondary haemorrhage (Fig. 8.6 )
264
8 Spleen and Pancreas
Fig. 8.5 Old splenic hematoma. Old splenic trauma: slight subcapsular fl uid with cyst-like
necrotic parenchymal areas after laceration
ab
Fig. 8.6 Splenic posttraumatic AVF. ( a ) Splenic posttraumatic AVF on CDS, with obvious
depiction of the red-coded feeding artery. ( b ) CDS depicts aliasing at the AVF and demonstrates
the draining vein encoded in blue
Role of US
Therapeutically splenic injury is increasingly managed conservatively or with
techniques that enable salvage of some splenic tissue. Thus imaging diagnosis, and
follow- up of splenic injury is particularly important.
Initially US most essential for depiction of free abdominal fl uid ( FAST ) – indication
for surgery usually based on clinical grounds and indication for additional imaging
usually based on trauma history and severity, complemented by US fi ndings.
NOTE : In early phase US may miss even signifi cant splenic injury, unless aCDS or
ce-US is performed.
8.1.10 Splenic Infarction
Defi nition
Rare condition in children, most commonly associated with sickle cell anaemia.
Other causes: acute portal vein thrombosis (venous infarction), infi ltration,
infl ammation and trauma.
8.1 Spleen
265
ab
c
Fig. 8.7 Splenic infarction. ( a ) Subacute splenic infarction in sickle cell anaemia: regional
alteration of tissue echogenicity reaching into periphery/subcapsular; some normal spleen tissue
left in the centre near the hilus. ( b ) Old splenic infarction – creates images similar to posttraumatic
changes, with cyst-like necrotic area. ( c ) aCDS demonstrates non-perfused, infarcted areas even in
a very early stage, where gray scale fi ndings may be very subtle or even not yet depictable
US Findings
Acute enlargement of spleen, initially even with normal echotexture. Secondary
heterogeneous inhomogenously patchy parenchymal echoes due to haemorrhage
and haemorrhagic infarction (Fig. 8.7a ). Increasingly hypoechoic-cystic aspect on
delayed imaging (Fig. 8.7b ).
(a)CDS
• Large/main infarcted vessels depictable by CDS
• Infarcted splenic tissue, particularly in early phase, often only detectable by
aCDS or ce-US (Fig. 8.7c )
8.1.11 Space-Occupying Lesions of the Spleen
8.1.11.1 Cysts
Defi nition
• Congenital – dysontogenetic, part of systemic cystic disease, posttraumatic and
postinfl ammatory (pseudocysts)
• Posttraumatic/infectious cysts may remain stable or diminish and resorb.
Congenital/systemic splenic cysts may grow concordant to spleen growth or even
more. In syndromatous or systemic cystic disease additional cysts may appear