Ebook Pediatric ultrasound: Part 2

(BQ) Part 2 book Pediatric ultrasound presents the following contents: Ultrasound of the chest, liver and bile system, spleen and pancreas, us of the gastrointestinal (GI) tract, ultrasound of the urogenital tract, small part and hip ultrasound.

M Riccabona, Pediatric Ultrasound,

DOI 10.1007/978-3-642-39156-9_6, © Springer Berlin Heidelberg 2014

M Riccabona

Division of Pediatric Radiology, Department of Radiology, University Hospital Graz, Auenbruggerplatz 3, Graz 8036, Austria e-mail: michael.riccabona@klinikum-graz.at

Contents 6.1 Requisites 190

6.1.1 Transducers 190

6.1.2 Positioning 190

6.1.3 Indications 190

6.1.4 How to Perform Chest US 191

6.2 Normal Findings 191

6.2.1 Chest Wall 191

6.2.2 Breast 191

6.2.3 Pleural Space 192

6.2.4 Diaphragm 192

6.2.5 Lung 192

6.2.6 Mediastinum 193

6.2.7 CDS 195

6.3 Pathology of Chest Wall 195

6.3.1 Aplasia, Variations of Ribs 195

6.3.2 Congenital Malformations 195

6.3.3 Traumatic Changes 195

6.3.4 Chest Wall Tumours 196

6.3.5 Breast 196

6.3.6 Role of US and Additional Imaging 198

6.4 Pathology of Pleural Space 198

6.4.1 Pleural Effusion 198

6.4.2 Empyema 198

6.4.3 Other Pleural Pathology 200

6.4.4 Role of Imaging 200

6.5 Pathology of Diaphragm 201

6.5.1 Diaphragmatic Hernia 201

6.5.2 Diaphragmatic Motion Disturbance 202

6.5.3 Role and Potential of Imaging 202

6.1 Requisites

6.1.1 Transducers

Chest Wall

High-resolution linear arrays, plenty of US gel (stand-off pad sometimes helpful)

Deeper Structures

Sector and curved linear arrays – small surface helpful to properly insonate through intercostal space for suffi cient penetration into deeper structures

Frequency depends on age and depth of targeted structure

6.1.2 Positioning

Depends on area of interest: prone, supine, decubitus

• For jugular access extend head and neck, potentially put pillow below

shoulders

NOTE : For standardised assessment and measurement of pleural effusions stan-dardised upright positioning (sitting) helpful – also improves comparability with chest radiographs 6.1.3 Indications • Pleural and pericardial effusions • Equivocal opacities on plain fi lm – e.g tumour, malformation, cyst, pneumonia and effusion

• Diaphragm and diaphragmatic motion 6.6 Lung Pathology 203

6.6.1 Pneumonia 203

6.6.2 Lung Abscess 203

6.6.3 Atelectasis 204

6.6.4 Respiratory Distress Syndrome (RDS)/Hyaline Membrane Syndrome 205

6.6.5 Sequestration 206

6.6.6 Congenital Cystic Adenomatoid Malformation (CCAM) 207

6.6.7 Cysts 207

6.6.8 Infarction 208

6.6.9 Tumours and Space-Occupying Lesions 210

6.7 Other Miscellaneous and Rare Applications 210

6.7.1 US for Interstitial Lung Disease 210

6.7.2 US for Pneumothorax 211

6.8 Additional Imaging 211

For other chest areas:

• Upper abdomen with transdiaphragmatic access through liver and spleen

• Subxiphoid access

• Jugular access

• Intercostal access

NOTE : In neonates and infants, ossifi cation of chest wall is not completed – access

through cartilaginous parts of sternum and ribs

Documentation: Basic minimum documentation of all scanned areas is advisable, even if normal If lesion, image in longitudinal and axial sections:

• Additional sections should be obtained if necessary and with pathology

• Try to document all relevant structures with some neighbouring reference structure

• Proper labelling, potentially using pictograms, is extremely helpful

NOTE : Even if only chest US is requested, orienting overview of cardiac

struc-tures or potential effusion (and upper abdominal “sonoscope” – brief survey

of particularly upper abdomen) is helpful Detailed course of investigation depends

Below chest wall:

• Echogenic surface – reverberation echoes caused by air-fi lled lungs

• In more medial position – cardiac and mediastinal structures

6.2.2 Breast

Breast appearance varies with age, depending on hormonal status:

• Neonatally breast tissue seen, may appear large, eventually regresses

• In (pre)puberty breast tissue increases, typical change in echotexture

• Eventually typical adult breast US features

NOTE : Some minimal breast tissue even in male neonates physiologic; thereafter

no breast tissue should be seen at any stage of development in boys

6.2.3 Pleural Space

Usually pleural space not accessible by US

Visualisation of both pleural sheets only achieved by high-resolution linear

arrays if some effusion present

NOTE : The two pleural surfaces move independently from each other

6.2.4 Diaphragm

Seen as un-/hypoechoic muscular structure – particularly at origin and insertion Majority of diaphragm usually only indirectly visible – by aerated lung surface:

• Movement/shape of diaphragm assessed using this pseudosurface

• With pleural effusion, even smaller parts of diaphragm visible

• Documentation of diaphragmatic motion: M-Mode, video clip (Fig 6.1 )

6.2.5 Lung

Normal lung is aerated and only seen indirectly by surface (echogenic structure with reverberation echoes that change with respiration)

• Parts beyond aerated lung surface not visualised

NOTE : As soon as US can penetrate lung tissue, some pathology must be expected

(e.g atelectasis, consolidation, effusion, other non-aerated space- occupying process)

Respiratory motion of lung surface used to differentiate normal aerated lung from pneumothorax, where no motion of refl ecting surface/air space can be noted:

• Also seen in air-fi lled bronchogenic cysts and severe obstructive hyperinfl ation

• Documentation by video clip or M-Mode

Basal parts of lungs best seen by transabdominal access:

• Should be part of any standard abdominal US (as effusion, atelectasis and pneumonia may cause abdominal complains, particularly in young children)

6.2.6 Mediastinum

6.2.6.1 Anterior Mediastinum/Thymus

Mainly Thymus (Fig 6.2 ):

• Physiologically large in neonates, then eventually regresses

• Shape and size variable

• Echogenicity: hypoechoic, mixed, with some septa (“dot-dash pattern”)

• Behaviour of soft tissue: not compressing or displacing other structures, particularly vessels

• Size of thymus diffi cult to assess, reliable age-related normal values not available

• CDS: some internal vascularity

• Additionally: ideal acoustic window to deeper structures

NOTE : Large thymus at unusual age may point at diffuse infi ltration or mus hyperplasia; infi ltration and tumours will cause increased stiffness and thus sub-sequent impression or displacement of surrounding structures or crossing vessels

thy-6.2.6.2 Middle Mediastinum

Contains – among others – large vessels, trachea, potential nodes may be visualised

by US (Fig 6.3 ):

• Particularly feasible in neonates and infants

Fig 6.1 Diaphragm and diaphragmatic motion: ( a ) Normal diaphragmatic respiratory motion on

M-Mode – the echogenic border represents air-fi lled base of lung, not diaphragm itself, the

inho-mogeneous spots are minimal peripheral atelectatic areas ( b ) No diaphragmatic motion,

conspicu-ously documented by M-Mode, after surgery and postoperative pleural effusion in diaphragmatic

palsy ( c ) M-Mode under respirator therapy: M-Mode trace refl ects effect of mechanical

ventila-tion and not patients’ own respiratory moventila-tion

Fig 6.3 Middle mediastinum: vessels and lymph nodes Parasternal (jugular) sagittal view, sector

transducer: thoracic aortic arch, supra-aortic vessels, two enlarged mediastinal lymph nodes (

dot-ted circular lines )

Fig 6.2 Thymus: ( a ) Anterior mediastinum, axial section, linear transducer: Large neonatal

thymus, serving as window to deeper structures such as the great vessels Note non-ossifi ed

sternum with central ossifi cation centre ( b ) Sagittal section, anterior and middle mediastinum,

linear transducer in trapezoid format, paramedian view: Large neonatal thymus Note anechoic non-ossifi ed parts of ribs and large, uncompressed vessels; behind one can see a feeding tube in the

oesophagus ( c ) Left anterior mediastinum, axial section, sector transducer: Enlarged thymus with inhomogeneous echogenicity in a child with Hodgkin lymphoma ( d ) Right anterior mediastinum,

axial section, linear transducer in trapezoid format: US in mediastinitis, abscess-like ous infl ammatory lesions with nodular appearance in the mediastinum

Except for assessment of vessels, CDS not very useful in normal situation

Indications for chest CDS for DDx in pathology mostly of the lung: e.g abscess

or necrosis, tumour vascularisation, vascular malformations, suspected particularly peripheral pulmonary artery embolism (PAE, resemble triangular subpleural pneu-monic areas without depictable vascularistion), etc

6.3 Pathology of Chest Wall

6.3.1 Aplasia, Variations of Ribs

Quite common, cartilaginous part nicely assessed by US, wide range of rib anomalies:

• 3DUS reconstructions improve understanding and visualisation (see Fig 1.34 )

• Plain fi lm: US complements plain fi lm

Fractures of ribs and sternum: see musculoskeletal US (Chap 11 ):

• Particularly in cartilaginous parts and sternum

– US may be superior to plain fi lm, where these structures are diffi cult to assess

if not signifi cantly displaced

NOTE : Follow entire structure in longitudinal and axial sections to detect any

sur-face interruption/irregularity

Often some reactive focal subperiosteal haematoma:

• Without history, differentiation from osteomyelitis diffi cult

• Particularly if bilateral, multiple, of different age – NAI should be considered Additional fi ndings:

• Complicated haemorrhagic pleural effusion, atelectasis

• Haematoma: seen in all chest wall spaces, usually no indication for imaging – only

in unclear cases, complicated course, suspicion of infection (DDx: seroma, etc.)

6.3.4 Chest Wall Tumours

6.3.4.1 Lymphangioma (veno-lymphatic vascular malformation)

US fi nding : Multicystic space occupying lesions with echogenic septae

• Spontaneous haemorrhages with fl uid-fl uid levels often present (see Fig 4.12 )

• CDS: potentially some vessels within septae

Rare; e.g rhabdomyosarcoma or Ewing sarcoma (Fig 6.5 ):

• Sometimes diffi cult to differentiate from myositis ossifi cans, particularly Askin tumour

US fi nding : No specifi c sonographic features

6.3.5 Breast

Breast US: In childhood of limited importance

Neonates : Transient physiologic swelling, cystic duct ectasia and cysts seen

• Secondary infection with abscess formation and haematoma may occur (Fig 6.6a )

( Pre -) puberty cysts, tubular duct ectasia, fi broadenoma, infl ammatory formations

(Fig 6.6b ):

• Overall appearance varies with age and maturation (Fig 6.6c )

• Most pathological entities do not differ from typical US appearance in adults

Additional application of breast US in childhood: Assessment of sexual maturation,

documenting presence and size of breast tissue

• In girls with suspected hormonal or genetic pathology

• In boys with gynaecomastia

– In some centres proof of signifi cant breast tissue necessary for treatment decision

NOTE : Breast carcinoma extremely rare in childhood

CDS : Can be helpful for assessment of superfi cial tumours or vascular malformations

and other pathology described in respective chapters

a

c

b

Fig 6.6 Breast US in childhood: ( a ) Neonatal breast abscess – huge collection with membrane

and adjacent soft tissue reaction (hyperechoic, swelling) after neonatal mastitis; note plenty US gel

to facilitate transducer coupling to tissue without interposing air ( b ) Impressive cystiform duct ectasia in a breast feed infant ( c ) Asymmetric prominent breast tissue at onset of pubarche in

11-year-old girl

6.3.6 Role of US and Additional Imaging

US : Supplementary tool in clinically equivocal situation, follow-up

Additional Investigations :

• Suspicion of tumour – depending on oncology protocols – plain fi lm, CT/MRI

• Assessment of osseous structures: plain fi lm, rarely CT

• Mammography: rarely indicated, and only in/after puberty

6.4 Pathology of Pleural Space

6.4.1 Pleural Effusion

Defi nition : Some fl uid in between two pleural sheets of varying aetiology:

• Cardiac, infl ammation, trauma, tumour, etc

• Most common pleural change, most common indication for chest US

US fi ndings :

Simple pleural effusion : Unechoic fl uid without septae (Fig 6.7 )

Complicated effusion : Fluid contains fl oating echoes, septae, complex nature (Fig 6.8 ):

• Depends on haemorrhage, chronicity and recurrence, empyema, etc

• Defi nite diagnosis of underlying entity not achievable by US

NOTE : Quantifi cation of pleural effusion limited If US used for follow-up

(to determine increase or decrease of amount of fl uid) – use standardised views and positioning:

• Possibly in sitting or upright position

• US aspect changes signifi cantly with posture – with redistribution of fl uid, depending on position

6.4.2 Empyema

Defi nition and US fi ndings : Complex effusion with multiple septae which may

contain vessels (Fig 6.8b ):

• Some space-occupying component

• May compress adjacent lung – often associated with or even caused by pneumonia, atelectasis and abscess

( a ) CDS : Peripheral and Septal Hyperaemia

DDx : Any other complex fl uid, most important entities:

• Subphrenic/subpulmonic abscess, lung abscess (may exist concurrently)

• Complex pericardial effusion

• Haemorrhagic bronchogenic cyst

• Complex echinococcal/hydatid cyst

• Thoracic lymphangioma

• Ventral meningocele (usually clear fl uid, posterior mediastinum)

• Duplication cyst

Fig 6.7 Simple pleural effusion: ( a ) Axial view: Small amount of simple pleural effusion (+ +)

in pleuritis: the little amount of effusion better visualised on US than on plain fi lm Note pleural

thickening ( b ) Sagittal dorsal view in upright sitting child for standardised assessment: simple pleural effusion – height (+….+) can be measured ( c ) Axial view through liver, transducer tilted

cranially: bilateral simple pleural effusions in a neonate – US cannot differentiate kind and entity (e.g chylothorax)

Fig 6.8 Complicated pleural effusion and empyema: ( a ) Axial intercostals view with sector

transducer: complex fl uid with fl oating echoes in complicated pleural effusion, lung compressed and not aerated; US does not allow for differentiation of entity (e.g haemorrhage versus

infl ammation) ( b ) Axial section: Complicated effusion with cystic areas in pleural empyema; NOTE : Atelectasis of adjacent pneumonic lung

6.4.3 Other Pleural Pathology

Thickening of pleura: after surgery/infl ammation

Space-occupying lesions/tumours of pleura: extremely rare in children

• Few entities reported:

– Pleural mesothelioma, pleural carcinosis, infi ltration by metastases

– Penetration from pulmonary as well as abdominal tumours (Fig 6.9 )

• Ideal complementary imaging tool for assessing equivocal opacities on plain fi lm

• May guide diagnostic/therapeutic aspiration/drainage (Fig 6.10 )

• Applicable at bedside, in ICU/NICU, ER, etc

Additional / Complementary Imaging :

• Plain fi lm, particularly in initial diagnosis, considered compulsory

• In complex situations CT, fl uoroscopy, MRI, scintigraphy and biopsy

• Gap in diaphragm: discontinuity may be diffi cult to visualise

• Indirect sign: abnormal shape, displacement of abdominal structures into chest:

– Particularly intestinal structures fi lled with fl uid (Fig 6.11 )

– Hiatal/Bochdalek hernia: fi ll stomach/intestines by liquid feed

– Without structural herniation: diffi cult to differentiate diaphragmatic eventration versus hernia, particularly on right side (liver covering defect, usually in fi brous part) (Fig 6.11c )

NOTE : Differentiation of small gap from eventration of diaphragm may be

impos-sible; same applies to reliable “exclusion” of diaphragmatic hernia

Fig 6.10 Pleural drainage/puncture: ( a ) Puncture needle ( arrow ) entering pleural space ( b ) Tip of

chest drain ( arrow ) visualised in some residual effusion with sedimentation after pleural haemorrhage

6.5.2 Diaphragmatic Motion Disturbance

Changes in diaphragmatic mobility easily seen:

• Documented by video loops or M-Mode (see Fig 6.1 )

• Correlation with respiratory manoeuvres: allows differentiation of relaxation from palsy or reduced mobility (e.g secondary to pneumonia or trauma):– Diaphragmatic palsy – paradoxical motion

– Relaxation – absent or minimal motion, but symmetric during respiratory cycle

NOTE : Assessment of diaphragmatic palsy should always be performed without

positive pressure ventilation (will mask abnormal motion)

6.5.3 Role and Potential of Imaging

US : primary tool in assessment of suspected diaphragmatic pathology

Additional imaging : plain fi lm, fl uoroscopy, cross-sectional imaging

• Only in equivocal situations

a

c

b

Fig 6.11 Diaphragmatic hernia: ( a ) Paramedian sagittal section in a neonate with diaphragmatic

her-nia – fl uid-fi lled stomach reaches up into left chest through defect, which is only partially covered by

liver ( b ) Axial transhepatic view tilted cranially behind liver muscular remnants of diaphragm seen – but dorsally, liver parenchyma and intestinal loops herniated into right thoracic cavity ( c ) Diaphragm

“bump” (eventration) on an axial oblique transhepatic/abdominal view tilted cranially

6.6 Lung Pathology

6.6.1 Pneumonia

Defi nition : Infl ammatory change of various reasons

• US appearance not specifi c in terms of aetiology

US fi ndings (Fig 6.12 ):

• Liver-like aspect of fully non-aerated lung tissue, some mass effect

• More or less echogenic stripes with tree-like appearance (sonographic air bronchogram):

– Potentially change with respiration

– Depend on amount of fl uid in bronchial structures

DDx : Dys-/Atelectasis, infarction, other infi ltration

6.6.2 Lung Abscess

Defi nition : Complication of infection and/or aspiration

US fi ndings : Seen if access possible (through pneumonic lung, etc.) (Fig 6.13 ):

• As any abscess elsewhere: complex cystic mass with membrane-like wall

• Potentially fl uid-fl uid or fl uid-air levels

CDS : No central vascularisation, well-vascularised hyperaemic capsule

• Potentially bronchial/pleural arterial supply particualrly with long history

DDx : Other complex cyst, necrosis (may be indistinguishable) and haemorrhage

Fig 6.12 Pneumonia Two typical images of pneumonia – with more or less perceived bronchogram and reactive pleural effusion

sonoaero-6.6.3 Atelectasis

Defi nition : Area of hypoinfl ation, if completely non-ventilated = atelectasis, if some

areas show residual ventilation = dystelectasis

US fi ndings : Similar to pneumonia – liver-like appearance of lung tissue, without

any central air echoes, collapsed aspect with concave surface (Fig 6.14 ):

• Potentially bronchial/vascular structures can be discriminated as tubular bands

• If residual air in central bronchi, sonographic air bronchogram seen:

– Similar to pneumonia

a

c

b

Fig 6.13 Lung necrosis and abscess Three conglomerating lung abscesses: Depicted on gray

scale ( a ) without perfusion on CDS ( b ) aCDS reveals more conspicuously vascularised and non- perfused necrotic areas ( c )

NOTE : These and pneumonic changes only visible when pathology reaches lung

periphery, becoming accessible for US

6.6.4 Respiratory Distress Syndrome (RDS)/Hyaline

Membrane Syndrome

Defi nition : Surfactant defi ciency, typically in preterm neonates due to immature

lung or secondary to surfactant consumption - results in secondary collapse of

alveolus NOTE : Possibly prediction of bronchopulmonary dysplasia (BPD) by

lung US: incomplete resolution of retrodiaphragmatic hyperechogenicity by the second or third week = high probability for BPD

US fi ndings : More or less inhomogeneous echogenicity from reduced ventilation –

varying degree of sound penetration, potentially changing with respiration allows some grading as well as assessment during follow-up:

• Higher echogenicity than in pneumonia or atelectasis, sometimes (mild RDS) only surface echo visible

• Potentially atelectasis-like appearance

• Other appearances: confl uent B-lines, pleural line and subpleural abnormalities without spared areas

Fig 6.14 Atelectasis: ( a ) Axial transhepatic view: atelectatic, echogenic, concave-shaped lung – compressed by pleural effusion ( b ) Sagital view: peripherally collapsed lung – minimal atelectasis

of dorsolateral lung with secondary effusion

6.6.5 Sequestration

Defi nition : Lung tissue without function, usually without connecxion to

tracheo-bronchial system Part of spectrum of various congenital lung/foregut tions (Fig 6.15a )

Usually atypical vascular supply:

• Commonly from aorta, potentially draining into systemic vein

• Typically positioned in lower lobes, particularly left sided

US fi ndings : Usually best seen from abdominal approach (Fig 6.15b ):

• More or less homogeneous, slightly echoic, space-occupying lesions

• May have complex inhomogeneous appearance with cysts (hybrid lesion)

• Large tubular structures often seen represent vessels

• Displaces lung, rarely also intraabdominal

a

Fig 6.15 Sequestration and lung malformations: ( a ) Schematic demonstration of the range

of foregut malformations, graded depending upon amount of tissue and/or vessel alteration

( b ) Typical sagittal US image of in this case an infradiaphragmatic echogenic sequestration in a neonate with right-sided diaphragmatic hernia NOTE : intrathoracic liver and slight effusion, as well as preserved part of diaphragm covering sequestration ( c ) CDS reveals the systemic vascular

supply, in this case deriving from a thoracic artery (chest wall vessel)

CDS : Commonly large-supplying artery deriving from abdominal aorta (Fig 6.15c ):

• Draining vein depictable if drains into abdominal inferior cava; allows differentiation of intra- versus extralobar sequestration

NOTE : Sequestration may also occur infradiaphragmatically

6.6.6 Congenital Cystic Adenomatoid Malformation (CCAM)

Defi nition : Part of spectrum of foregut malformations (see Fig 6.15a ) Typically three types differentiated, depending on cyst size:

• Type 1 = large cyst(s) > 2 cm

• Type 2 = multiple medium-sized cysts around 1 cm

• Type 3 = pseudosolid mass with multiple microcysts not resolvable by US

US fi ndings : More or less echoic, complex mass (Fig 6.16 ):

• Varying number and size of cysts depending on type

• Between cysts there can be echogenic septae

CDS : No large vessels, some vascular supply sometimes seen

DDx : Atypical form of sequestration, hybrid lesion, bronchial atresia with non- aerated malformed lung tissue, if more homogenous - thoracic kidney (usually

in the dorsal paramedian basal part of the chest)

Fig 6.16 CCAM: CCAM type I (large macrocysts, + +) – diffi cult to differentiate from other

fl uid fi lled/cystic mass (bronchogenic, cystic sequestration, etc.)

6.6.7 Cysts

Defi nition : Fluid- or (if connected to tracheobronchial system) air-containing lesions:

• Seen only if positioned close to lung surface

US fi ndings : Simple cyst(s) of varying size (Fig 6.17a ):

• Posterior acoustic enhancement, smooth surface

• Separation from other entities diffi cult

• If fi lled with air, bright reverberation echoes without change during respiratory cycle, thus distinguishable from normal lung (Fig 6.17b )

• Bronchial cysts – potentially air-fl uid levels (may be diffi cult to depict) (Fig 6.17c )

DDx : Echinococcus/hydatid cyst (focus on typical wall appearance):

• Complicated cysts (echoes within lumen, aetiology not defi nable by US)

• Pericardial/pleural cysts

• Postinfl ammatory cysts, abscess, AV-malformation (use CDS)

6.6.8 Infarction

Defi nition : Pulmonary artery embolism PAE

US fi ndings : Pneumonia-like subpleural triangular areas without perfusion

• Usually hypoechoic, liver-like appearance, often relatively homogeneous:– Beginning – some ventilation possible

– Later stage – completely resemble pneumonia, but no pulmonary vessels depicetd by (a) CDS

CDS : No central vascularisation/fl ow, no pulmonary vascular supply (Fig 6.18 ):

• Some pleural vessels may be depicted

NOTE : Perfusion defi cit for other reasons (cardiac, postoperative, etc.) sometimes

diffi cult to distinguish, but tends to be more global, with less pronounced changes

of the lung echotexture

e

Fig 6.18 PAE and pulmonary perfusion defi cit: ( a ) Axial view, infant after Glen procedure – with peripheral pneumonia-like oedematous lung ( b ) Same child as in ( a ): note severe postoperative perfusion defi cit of one lung ( c ) Axial view through liver: Large infarction, no air sonobroncho- gram as would be seen with infection ( d ) Dorsal scan through intercostals space: triangular sub- pleural pneumonia-like lung area, typical for infarction induced pneumonia ( e ) CDS demonstrates

lack of perfusion in the peripheral triangular subpleural consolidation

Fig 6.19 Lung tumour Axial view: chest fi lled with partially cystic tumour that turned out to be

a pulmonary blastoma

6.6.9 Tumours and Space-Occupying Lesions

Defi nition : Lung tumours rare in children US has limited role:

• One may visualise tumours if reaches lung surface

US fi ndings : US fi ndings vary depending on tumour and composition (Fig 6.19 ):

• More or less echogenic, potentially necrotic areas or calcifi cations

• Sometimes origin depictable – allows speculation on aetiology

CDS : Evaluate vascularisation, depict necrosis, asses supplying/draining vessels:

• Pneumonia, atelectasis: CDS helpful for showing normal vascular supply allowing differentiation from infarction or depiction of necrotic area before typical abscess formations manifest

• Superfi cial/pleural/soft tissue arteriovenous malformation: CDS irreplaceable for diagnosis

DDx : Any other cause of non-aerated lung, particularly CCAM, sequestration,

pneumonia, abscess, complicated cysts and hernia:

• In medial/mediastinal aspect: thymus versus lymphoma, etc

• Extremely rare intrathoracic kidney (normal kidney in atypical location):

– Typical renal vascularisation pattern – undisputable diagnosis

6.7 Other Miscellaneous and Rare Applications

Many More Partially Rare Applications Reported: Most Relevant Ones

6.7.1 US for Interstitial Lung Disease

Increased extravascular lung water creates “B-line” on lung US; a few B-lines can be found in a healthy population:

NOTE: False-positive fi ndings from hyperextended hyperinfl ated lung (COPD,

severe asthma, aspiration with focal emphysema/hyperinfl ation, etc.)

6.8 Additional Imaging

Plain fi lm, CT, sometimes (and increasingly) MRI:

• Rarely angiography (vascular malformations) or fl uoroscopy

• Role/value of US exquisite for follow-up of effusions or diaphragmatic palsy:

– Image-guided interventions: diagnostic or therapeutic puncture (in effusions, abscess, chylothorax, haematothorax, tumour biopsy, etc.)

NOTE : US has limitations in the chest – complementary imaging tool Plain fi lm

often initially compulsory US often used in equivocal fi ndings (e.g white thorax) (Fig 6.20 ) Always include assessment of lung base in upper abdominal US and FAST examinations.

haemi-b a

Fig 6.20 Case examples where US was helpful to further defi ne the cause of equivocal chest fi lm

fi ndings: ( a , b ) White haemithorax on chest fi lm ( a ): US ( b ) reveals a partially atelectatic, partially

pneumonic lung with elevated position of the diaphragm The pulmonary vessels are well

perfused on CDS, no sign of tumour, only slight effusion ( c ) Atypical opacifi cation of right lower lung on plain fi lm: US ( d ) demonstrates collapsed lung with secondary pneumonic changes

in a child after aspiration

M Riccabona, Pediatric Ultrasound,

DOI 10.1007/978-3-642-39156-9_7, © Springer Berlin Heidelberg 2014

M Riccabona

Division of Pediatric Radiology, Department of Radiology,

University Hospital Graz, Auenbruggerplatz 3,

7.1 Requisites and Investigation

7.1.1 Preparation

Fasting helpful for suffi cient fi lling of gall bladder and bile duct assessment Additional provocation by feeding during investigation helpful to enhance visu-alisation of intrahepatic and extrahepatic bile ducts and allows for assessment of gall bladder emptying

For quantitative assessment of liver perfusion (portal vein velocity and hepatic artery fl ow), child must be fasted to avoid fl ow alterations from increased splanch-nic fl ow mimicking pathology or masking disease

TIP : Fasted means no food, no drink, no chewing gum, no sweets, no smoking, etc

7.1.2 Positioning

Conventionally supine position

• In small children positioning manoeuvres diffi cult

• Potentially intercostal access necessary

• In older children manoeuvres can be attempted, instructing child “to show a big tummy” or similar child-adapted wording

NOTE : For improving lesion detection and characterisation, IV ce-US particularly

helpful – although currently no US-CM registered for paediatric use

7.1.4 Course of Investigation

Liver usually assessed from ventral and lateral, rarely dorsal approach necessary or helpful Systematically sweep through entire liver in sagital, axial and oblique sec-tions follow course of major structures (portal nvein liver veins), assess gall blad-der, and eventually add Doppler if indicated

Small children do not respond to positioning commands – use respiration or ask them to “take deep breath” may enable assessment, particularly of subdiaphrag-matic areas

particu-• Standardised documentation (VAL – defi ned by upper pole of right kidney, MCL – commonly defi ned by gall bladder, STL – defi ned by abdominal aorta), section through hepatic veins, portal vein branching, main portal vein (if not included gall bladder view) (Fig 7.1 ) ( www.oegum.at )

NOTE : Due to complexity of the liver, documentation and measurements in

standardised sections are essential For identifi cation of section – include other key structures on image, particularly important for comparison during follow-up

7.2 Normal Findings

7.2.1 Structure

Liver has larger right and smaller left lobe, internal architecture classifi ed by liver segments (Fig 7.1 )

Parenchyma – homogenous echo of medium echogenicity, contour and borders

as well as sharp and smooth margins Size varies with age, particularly height – measurements correlated with normograms (Table 7.1 )

NOTE : Physiologically left liver lobe is much larger in neonates than in older ages;

it gradually shows relative decrease in size after closure of ductus venosus

a

b

Fig 7.1 Standard liver measurements and liver segments: ( a ) Liver anatomy with liver segments

( I – VIII ), relevant liver vessels for anatomical classifi cation (portal vein, hepatic vein, inferior vena cava) and standard planes for US measurements, particularly right anterior axillar line ( AL ), right and left middle clavicular line ( r / lMCL ) and medially positioned sterna line ( STL ) Two respective

normal sagittal views with important reference structure (upper pole of right kidney for AL,

abdominal aorta for STL) given ( b ) Standard image appearance of typical liver sections: the

trans-ducer position and orientation given in the schematic drawing, with respective US images

varied insertion at different levels of intrahepatic ICV exist as normal variants Size may vary with respiration and intravascular volume – usually exhibit smooth border and straight course, with relatively thin low echogenicity wall

7.2.4 Portal Vein (PV)

Enters at hepatic hilus, should not show tapering (a sign of portal hypertension) Branches between left and right PV in liver centrally, left PV shows focal ectasia (Rex recessus, sinus venosus) at area of former insertion of umbilical vein draining via venous duct of Arantii (ductus venosus) to right atrium during fetal circulation Wall slightly more echogenic, partially increased by periportal structures (bile ducts, accompanying arteries) Periportal region gets enlarged and more echogenic

in various conditions or may appear prominent with decreased echogenicity of liver parenchyma

NOTE : In neonates (during fi rst weeks of life), communication may persist between

sinus venous and ICV/right atrium (“physiologically persistent ductus venous” Fig 7.2a ) – should obliterate spontaneously Persistent ductus venosus usually indi-cates underlying liver disease with increased peripheral liver resistance Umbilical

Table 7.1 Normal liver size in relation to age/height

Measurements of body height related (cm) normal liver size (cm) during childhood

vein may be visible in neonates physiologically, but shows no fl ow – consequently thromboses and vanishes; persisting (inverted) fl ow in umbilical vein – sign for portal hypertension and consequent portosystemic shunt A nonfunctioning umbili-cal vein catheter may end in this vein – actively search for it (Fig 7.2b ).

7.2.5 Hepatic Artery (HA)

Can be followed from its origin at coeliac trunk parallel to PV to branching into left and right HA

Usually CDS enables easy identifi cation and differentiation from other tubular structures, particularly in liver periphery, where differentiation of HA from (dilated) intrahepatic bile ducts is otherwise diffi cult

NOTE : Numerous normal variants in HA anatomy, e.g accessory left HA from

coeliac trunk or gastric artery, separate origin of right HA from superior mesenteric artery CDS particularly valuable for assessing these anatomic variants

7.2.6 Gall Bladder

Positioned on lower surface of liver, centrally close to hilus on right side Usually shows thin wall, contents unechoic Size can vary with time since feeding Best seen

in subcostal oblique view in MCL

NOTE : An empty or poorly fi lled gall bladder, particularly if relatively large when

fi lled, may show a pseudothickened wall (Fig 7.3a )

7.2.7 Common Bile Duct (Commonly Addressed

as Hepato- Choledochal Duct)

Usually crosses main PV and runs through head of pancreas to papilla/ampulla of Vater

Fig 7.2 Neonatal liver: ( a ) Physiologic persistent ductus venosus (+ +) ( b ) Flow and patency of

neonatally persistent ductus venosus depicted by CDS – fl ow direction documented by Doppler

trace ( c ) Still visible umbilical vein with catheter ( arrow )

NOTE : Duct (even ductus cysticus) often visible using high-resolution linear

trans-ducers (Fig 7.3b, c )

7.2.8 Intrahepatic Bile Ducts

Course parallel to PVs – usually only depicted centrally or if dilated

7.2.9 Doppler Findings

7.2.9.1 Hepatic Veins (HV)

Show bi- or triphasic undulating fl ow pattern, bidirectional fl ow direction Undulation caused by respiration and heart cycle (Fig 7.4a ) Absence of typical pattern usually indicates either increased liver resistance or increased right atrial pressure/volume overload

NOTE : Flow profi les may vary within the three main veins, also depends on point of

insertion and manoeuvres used for visualisation (such as breath holding) Undulation must always persist; bidirectional or triphasic pattern may physiologically be absent

7.2.9.2 Portal Vein (PV)

Usually shows constant fl ow into liver with some mild respiratory modulation (Fig 7.4b–d )

Flow velocities vary with age (Table 7.2a ) and fasting status

NOTE : Also intrahepatic PV branches should be assessed to show patency of at

least main right and main left PV Flow velocity measurements strongly rely on proper angle correction and good insonation angle (<60°)

7.2.9.3 Hepatic Artery (HA)

• Less often important

• Systolic velocity varies with age and nutritional status (Table 7.2b ), as does stolic velocity/RI

Fig 7.3 Bile system: ( a ) Normal, nearly empty gallbladder (+ +) with pseudothickening of wall ( b ) Normal common hepatic duct ( 3, 2 + +), confl uence with cystic duct ( 1 + +) ( c ) Axial sec-

tion shows pancreatic portion of prominent common bile duct

• CDS essential for differentiating particularly peripheral branches from biliary structures and for proper angle correction (if fl ow velocity measurements taken)

NOTE : HA shows same fl ow direction as portal vein – only by selecting proper

CDS settings (gate, fi lter, fl ow velocity) – discrimination of PV and HA feasible on CDS

7.2.10 Special Aspects of Newborns and Infants

• After closure of ductus venosus – relative increase in size of the right liver lobe – neonates have signifi cantly larger left liver lobe than older children Left and right liver lobes may even be similar in size

• Newborns’ liver softer and more fl exible – slightly rounded lower margin is physiologic

• Parenchyma less differentiated and less echogenic than in older age due to reduced fi brosis and less fat – compared to renal cortex liver parenchyma echo-genicity is lower

a

d

Fig 7.4 Liver vessels: ( a ) Hepatic veins, bidirectional undulating fl ow demonstrated by CDS

(either red or blue signals indicating two fl ow directions during respiratory cycle) with cardiac and

respiratory modulation also demonstrated by spectral fl ow analysis ( b ) Main portal vein entering

liver: note no signifi cant variation in diameter ( c ) Portal vein fl ow on CDS ( red colour signals ): note adjacent hepatic artery with faster fl ow in same direction (coded in orange ) ( d ) Duplex-

Doppler fl ow profi le confi rms normal hepatopetal portal fl ow +1 indicates maximum velocity

0–5 3.5 ± 2 9.1 ± 70 ? a ? (85 ± 15) a 6–12 6.3 ± 2 13.4± 250 ? (50–100) a ? (60 ± 10) a >12 7 ± 2.6 14.6 ± 5 380 70–120 60 ± 4 Average values are not applicable, as velocities are very low in neonates (around 40 cm/s), even lower in preterm babies, and increase relatively quickly to values similar to older

children – HA hepatic artery, PV portal vein

(d) typical fl ow patterns of heaptic veins

Type I Normal Triphasic, bidirectional

fl ow

EI ~ 120 % Type II Unspecifi c Triphasic, monodirec-

tional fl ow

EI ~ 90 % Type III Dampened Tonodirectional, but

still modulated fl ow

EI ~ 40 % Typ IV Severely

impaired

Monodirectional, uniform, unmodulated

fl ow

EI ~ 0 %

• Periportal echoes less prominent

• Ductus venosus can remain patent up to some weeks – seen as tubular vascular structure coursing from ectatic section of left PV to ICV/right atrium Closes spontaneously – then seen as echogenic band (= ligamentum venosum in later age) (see Fig 7.2a, b )

• Unusual or altered fl ow patterns in neonates do not always indicate hepatic ease; often refl ect physiologic systemic or vascular variations (e.g patent fora-men ovale, PDA, persistent ductus venosus Arantii) Interpretation of Doppler

dis-fi ndings needs to be made with care and respect to all other clinical and tory data as well as imaging fi ndings; sometimes additional assessment of abdominal aorta, renal or cerebral vessels, heart and other large vessels neces-sary for deciding on origin of unusual fl ow fi ndings

labora-7.3 Pathology of the Liver

7.3.1 Congenital Changes and Normal Variance

7.3.1.1 Situs Inversus (Abdominalis)

7.3.1.3 Hypoplasia/Atrophy of Left Liver Lobe and Other Variations

Hypoplasia is usually a consequence of intrauterine events – not congenital or hereditary, only conatal malformation

Other variants are diaphragmatic bump fi lled with liver, variations associated with diaphragmatic hernia and liver up-position, variations associated with gastros-chisis and omphaloceles

Many variations both of arterial and venous anatomy are most identifi ed by proper technique using CDS Have little other implication – unless liver surgery or transplantation planned

lower margin slightly rounded Echogenicity more or less decreased, with normal appearance of periportal area, unless signifi cant decrease in parenchymal echo-genicity – then periportal regions become prominent Associated oedematous changes of gall bladder wall and bed possible (DDx: cholecystitis, congestive, vas-culitis such as Kawasaki disease, during intensive care)

Associated fi ndings: enlarged lymph nodes in hepato-duodenal ligament, splenomegaly

CDS

Hyperaemia with low RI of HA, potentially increased PV fl ow; in severe ment and thus increase in liver resistance also reduced undulation in HV

NOTE : US does not allow defi nition of aetiology or discrimination between viral,

bacterial, toxic, drug-induced or other forms of hepatitis/hepatopathies Mimics exist

7.3.2.2 Liver Abscess

Defi nition

Usually haematogenous, sometimes ascending through bile ducts

Various entities – bacterial, fungus, secondary after malignant infi ltration, coccal or other parasites (amoebiasis, ascariasis, schistosomiasis, etc.)

US Findings

Spherical or polygonal focal alteration of liver texture If necrotic – central hypoechoic, sometimes with (fl oating) echoes, in complex abscess formations increased central echogenicity, fl uid levels Usually peripheral membrane and halo- like peripheral hypoechogenicity (Fig 7.5 )

Image varies with course – only subtle fi ndings in beginning, more pronounced

Special Entities :

• Echinococcal/hydatid disease: manifest as cystic liver lesions; different ances depending on age and stage (Type I –Type IV, Gharbi classifi cation used most commonly) (Table 7.3 ) (Fig 7.6 ) In children Type I and III commonly seen (younger manifestation) Differentiation of Type I lesion from other hepatic cysts diffi cult US used for puncture and therapeutic alcohol/drug instillation

Fig 7.5 Liver abscess ( a ) Focal nodular hypoechoic disruption of liver parenchyma and several

initial small lesions – in this case fungal septicaemia in oncology patient during chemotherapy

(fungal abscess) ( b ) CDS may confi rm the necrotic avascular nature and show peripheral,

mem-brane-like hypervascularisation

Table 7.3 Hydatid disease – grading system (Gharbi classifi cation)

Type I: pure simple cystic fl uid collection

Type II: cystiform fl uid collection with split, nodular-irregular wall; may contain echoes in central compartment

Type III: cyst with complex fl uid collection and internal septae

Type IV: cyst with heterogenous echo pattern, potentially beginning calcifi cations

Type V: cyst with refl ecting thick walls (mature/old form), often has calcifi ed walls

fi ne needle aspiration/biopsy Similar appearance seen in tuberculosis, sarcoidosis, metastatic disease, lymphoma or in patients with (acquired) immune defi ciency syndromes (the latter often with very mixed liver manifestation)

7.3.2.4 Role of US

• Nonspecifi c in infl ammatory liver conditions

• May be useful initially for narrowing down DDx or excluding other conditions that may cause similar symptoms

• Used for follow-up, particularly in chronic conditions

• Used for guided diagnostic punctures/therapeutic drainage/drug instillation

• Additional clinical and historical data, serologic diagnoses or search for pre- existing or causative conditions always essential

7.3.3 Other Parenchymal Liver Disease

7.3.3.1 Hepatopathy

Defi nition

Nonspecifi c fi nding, seen in a number of conditions such as secondary to drugs and treatment (drug induced/toxic damage) or secondary to systemic or metabolic dis-ease May be restricted to liver (e.g., Wilson disease, Gilbert syndrome) or systemic (e.g., glycogen storage disease, tyrosinaemia)

US Findings

Liver usually slightly enlarged with slightly increased echogenicity, may have some inhomogenicity of parenchyma with a more or less nodular pattern, without inter-ruption of normal straight and smooth vascular architecture

Fatty Liver/Steatosis

Defi nition

Rare in early childhood – mostly secondary to pre-existing liver condition or liver damage

Increasingly observed in adolescence due to obesity

Secondary to other systemic disease/treatment or drug induced

US Findings

• Large liver, maintained smooth surface, but lower margin rounded

• Echogenicity increases, structure commonly remains homogenous – focal totic areas usually occur along PV branches, but also elsewhere; inhomogenous steatosis possible, as well as areas of non-steatosis (Fig 7.7a )

stea-• Due to high attenuation, there is decreased penetration of sound, increasing nal loss and noise in deeper compartments Sound attenuation used for grading severity of steatosis

sig-• Potentially poor HV visibility

NOTE : Focal non-steatotic areas of normal tissue appear like focal liver lesions in

fatty liver (Fig 7.7b, c ) Commonly of lower echogenicity, spherical or polygonal shape, often in segment IV – do not show any change of contour or alter course of vessels, which helps for DDx Occasionally regional adenomatous hypertrophy of normal liver may occur (particularly in children after chemotherapy, who also may develop liver adenoma)

Liver Congestion

Defi nition

Occurs in conditions with increased right atrial pressure (secondary to congenital cardiac malformations, other cardiac disease, chronic respiratory insuffi ciency with increased intrapulmonary pressure such as cystic fi brosis), and secondary to intensive care with volume overload and increased right atrial pressure

US Findings

• Enlarged liver, initially reduced echogenicity

• In longer duration/chronic state – increased echogenicity

• Smooth surface, rounded lower margin, dilated HV that can be followed into liver periphery and showes reduced or lack of size modulation

• Ascites, splenomegaly, omental thickening and oedematous thickening of gested bowel wall – secondary signs

Defi nition

Either congenital genetic condition (e.g ARPKD) or consequence of chronic tions (cholestatic/infl ammatory) Rarely isolated entity or disease

US Findings

• Initial/mild manifestation – not visible

• With increasing severity and duration – increasing echogenicity of periportal areas with narrowed and potentially irregularly shaped peripheral PV branches –

7.3.3.3 Cirrhotic Liver

Defi nition

Main reasons in childhood: bile duct hypo-/aplasia, extrahepatic bile duct sis, α1-antitrypsin defi ciency, various metabolic diseases (Wilson disease, tyros-inaemia, cystic fi brosis, etc.), chronic intoxication (e.g copper), drug induced, after hepatitis, liver fi brosis/choledochal cysts, Caroli syndrome and other ciliopathies

Fig 7.8 Liver fi brosis – “starry sky” appearance

Strikingly increased periportal fi eld echogenicity

with irregular structure from biliary fi brosis

US Findings

Several states during course of disease (Fig 7.9 ):

• Initially increasing size, no other specifi c fi ndings

• Then decrease of liver size Irregular surface (varies with macro- and lar forms), convex shape of very sharp lower margin, increased inhomogenous echogenicity with reduced sound penetration, patchy parenchymal structure with focal nodular regeneration

micronodu-• Caudate lobe commonly spared – develops compensatory hypertrophy, ing spherical and of lower echogenicity (See Fig 7.9b )

becom-• HV and eventually PV become tapered, narrowed and intrahepatically ished – with irregular course and margins

dimin-• Secondary chronic changes: decreased size of gall bladder with thickened wall, splenomegaly, ascites and other fi ndings associated with portal hypertension

CDS

Essential for showing portal hypertension (see below) – usually intrahepatic form in cirrhosis Extrahepatic dilatation of PV with tapering at hilus as well as rarefi ed intrahepatic PV branches Secondary compensatory hypertrophy of HA which becomes large and very pulsatile Increased arterial perfusion secondary to reduced portal venous fl ow

surface and ascites in severe liver cirrhosis in an adolescent awaiting liver transplantation