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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5795_Библиотеки_им_академика_М_И_Перельмана.pdf
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M. Riccabona
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Fig. 14.4 HPSt. (a) Longitudinal section through pylorus, right paramedian upper abdomen:
enlarged pylorus, thickened wall (arrowheads), enlarged diameter (+ +) and length (× ×) and nar-
row canal (arrow). (b) Axial section through pylorus, right paramedian upper abdomen: enlarged
pylorus appearing as a round pseudotumourous lesion (arrow) with a central target sign. Thickened
wall (arrowheads), enlarged diameter (+ +). (c) Longitudinal section through pylorus, right paramedian upper abdomen: elongated pylorus within thick wall and ”pyloric shoulder” appearance of
gastric outlet with heavy peristalsis. Narrow canal, only minimal uid in duodenal bulb. (d)
Pylorospasm: longitudinal section through pylorus in right paramedian upper abdomen depicts
HPSt-like appearance, only beginning and end of pylorus intermittently open. Central spastic part
resolved after some time—then relatively normal passage into duodenum could then be observed
Note Reliability for assessment of sliding hernias and anatomic stomach anoma-
lies restricted.
Additional Imaging
pH monitoring for GOER (only useful in acid reux), oesophageal manometry and
uoroscopy (barium swallow).
14.1.6.2 Hypertrophic Pyloric Stenosis (HPSt)
Definition
HPSt best diagnosed sonographically.
Cramps with propulsive non-bilious vomiting. Typically occurs in boys aged
4–12 weeks.
Treatment usually by surgery, though medical conservative treatment may be an
option in early and mild disease with high surgical risk.
DDx
Pyloric atresia, gastric web, pylorospasm and gastric outlet tumours.
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US Findings
• Enlargement of pylorus and particularly pylorus muscle consistently throughout
investigation. Length >15mm, muscle >3mm, axial diameter ≥12mm and wall
lumen ratio >2:1 (Fig.14.4a, b).
• No or only minimal opening of pyloric canal (Fig.14.4c).
• Change in wall thickness from stomach to pylorus with typical shoulder-like
contour at pyloric entrance.
• Often displacement of pylorus, gastric enlargement with residual volume in
fasted children.
• Particularly after feeding, hyperperistalsis and secondary GOER.
• In late stages hypotonic enlarged stomach.
Note In early stages very young infants/preterm babies ndings may be subtle,
only functional observation + follow-up will establish diagnosis; sometimes difcult
to differentiate from pylorospasm (Fig.14.4d).
Follow-up under medical treatment:
• First no morphologic changes, but improvement of gastric clearance and content
passage to duodenum.
• Thickening and elongation may persist for several weeks (as also after surgery).
• Documentation of pyloric passage best by CDS and video clips.
Role of US
Main method for diagnosis, rarely in equivocal ndings uoroscopic UGI or MRI
for gastric tumours may become indicated.
14.1.6.3 Other Stomach Conditions
Gastritis/Ulcers
Not diagnosed by US, sometimes contour alterations can be seen in thickened stomach wall, provided sufcient lling without overlying gas/air. More easily visible if
adjacent deep abscess.
Bezoars and Foreign Bodies
Bezoars usually nicely assessable by US, foreign bodies if stomach lled
sufciently.
Appearance depends on content, bezoars typically with very echogenic surface
without sound penetration.
Hyperplastic Gastric Mucosa
Similar to gastritis—also potentially difcult to see.
May cause gastric outlook obstruction (severe mucosal thickening, young age—
typically neonates under prostaglandin therapy for PDA).
Menetrier’s Disease: Giant Hypertrophy of Gastric Mucosa
Typically affecting older children.
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M. Riccabona
US Findings
US may exhibit irregular thickened echogenic mucosa, particularly in fundus and
body of stomach.
Gastric muscle may also be thickened and hyperechoic.
Secondary ndings due to hypoproteinaemia (protein loosing enteropathy), such
as oedema, ascites and pleural effusions.
Eosinophilic Gastr(oenter)itis
Not differentiable from other types of gastritis—thickening of stomach wall including pyloric muscle, elongation of pyloric canal—may mimic pyloric stenosis.
Gastric Perforation
Complex regional uid collections at site of perforation.
Secondary changes such as ascites, peritoneal abscess and pneumoperitoneum.
Often underlying focal stomach changes may become visible, e.g. thickened
wall, (“ring-down”) artefact at site of perforation.
Granulomatous Disease
Any granulomatous disease may affect stomach.
Chronic granulomatous disease of childhood (x-linked disorder), most common
ndings include lymphadenopathy, hepatosplenomegaly, abdominal pain and
potentially pneumonia.
Stomach most commonly involved part of GI tract.
Seen as circumferential wall thickening and luminal narrowing.
May appear as benign masses in stomach wall.
Duplication Cysts
Characterised by its wall “gut signature” (see below—bowel), exhibiting typical
wall structure of related part of intestine. May have a connection with lumen.
US Findings
Usually unilocular cystic thick-walled lesions (see Fig.14.13). Have common blood
supply with organ of origin, move together with organ or its peristalsis.
Content echogenicity may change secondary to haemorrhage, infection, proteinous debris, epithelial cells and sediment.
Size variable—if connection with bowel lumen (see Fig.14.14).
Teratoma
Rare. Depending on histological composition may exhibit complex structure or
appear purely cystic with nodular-solid components/wall.
There may be calcication, bone, fat and secondary changes.
Focal Foveolar Hyperplasia
Rare gastric mass due to obstruction or inammation of gastric fovea (pits in
mucosa, where gastric glands empty).
14 US oftheGastrointestinal (GI) Tract
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US Findings
Echogenic polypoid masses in mucosal location.
Inflammatory Pseudotumour
A benign inammatory pseudotumourous mass, commonly in greater curvature
(also called plasma cell granuloma or broxanthoma).
US Findings
Often poorly dened with mixed echogenicity and secondary haemorrhage or necrosis.
Rare diffuse manifestation with diffuse hypervascular wall thickening—with
regionally enlarged nodes.
Other Benign Tumours
Many entities possible, though extremely rare (e.g. myobroma, polyps, haematoma, neuromyoma, neurobroma, haemangioma and lipoma).
US Findings
Tumour visible—entity cannot be dened/distinguished.
Diagnosis usually requires biopsy.
Malignant Masses
Most commonly lymphoma or gastrointestinal stroma tumours (GIST)—both manifest as single or multifocal masses.
US Findings
US depicts polypoid tumour or focal wall thickening that may mimic any other
space occupying lesion:
• Lymphoma: mass usually hypoechoic to normal gastric wall echogenicity, exhib-
its changes such as splenomegaly and enlarged lymph nodes, often relatively
large tumour at diagnosis.
• GIST: smaller at diagnosis, often heterogeneous and echogenic masses with
nodular and cystic areas (haemorrhage, necrosis).
Other rare gastric wall tumours: leiomyosarcoma, carcinoma (as familial/inherited
condition).
Diagnosis relies on histology.
14.1.7 Role ofUS
May depict ndings, but less reliable for ruling out conditions or specic entity
diagnosis—except for GOER, HPS and duplication cysts.
Additional Investigation
Endoscopy, MRI/CT, for some condition uoroscopy and biopsy.
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M. Riccabona
14.2 Bowel
14.2.1 Preparation andRequisites
Indications
Suspected intussusception, volvulus, necrotising enterocolitis, intestinal Henoch–
Schonlein purpura, appendicitis, inammatory bowel disease (Crohn’s, ulcerative
colitis, etc.), bloody diarrhoea, acute abdomen (e.g. after trauma), other nonspecic
queries, familial conditions (intestinal polyposis), during chemotherapy, etc.
Preparation and US Options
Acute US performed without specic preparation, particularly in query intussusception, volvulus and appendicitis.
Visualisation improved by oral uid intake, potentially with some distending
substances (as also used for MR-enteroclysis)—this allows proper distension and
good visualisation of lumen, detection of stenotic areas and intraluminal pathology
such as polyps.
Rectal enema (hydrocolon—“US enema”) with warmed saline solution, improves
assessment of colon for content, patency and distendibility; can also be used therapeutically for reduction of intussusception or meconium ileus.
Perineal access (after enema) for assessment of defecation and rectal/anal stenosis/atresia/malformation. Sometimes enema improves visualisation of stulae in
inammatory bowel disease or complex malformations.
Graded compression technique advised, positioning manoeuvres helpful for
transporting uid to area of interest.
Positioning
Usually supine, relaxed abdominal wall musculature helpful (can be achieved by
support to knees).
Transducers
Linear transducers with highest achievable frequency for optimal resolution helpful.
Curved linear arrays allow better overview, or extended view techniques. Sector
transducers rarely helpful.
Frequency depends on patient age and position of targeted bowel segment. The
smaller and the closer to surface, the higher the frequency (e.g. in neonates 15MHz,
in school children for appendiceal assessment 10–5 MHz).
14.2.2 Course ofInvestigation
Approach
Transabdominal + perineal.
Also access from ank and through full bladder/full stomach.
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Orientation
Helpful to rst assess in organo-axial section.
Identify well-dened structures (e.g. pylorus, gastro-oesophageal junction, coecum, rectum).
Follow respective loops continuously from distal to proximal.
Assess bowel wall (thickness, structure), size (stenotic part?), peristalsis and
compressibility.
Assess lumen and content. Bowel structure may help identication (jejuna folds,
colon haustrae, etc., Figs.14.5 and 14.6).
Add longitudinal sections for documentation of inner contour (folds) and assessment of stenotic segments (extended eld of view helpful).
Always assess surrounding structures (mesentery, lymph nodes, etc.).
Fig. 14.5 Schematic drawing of bowel appearance with respective typical pathology. Left side:
schematic drawing to demonstrate typical bowel features that may help to identify the various
bowel segments; this may physiologically not apply to (preterm) neonates due to immaturity (no
typical haustrae). Right side: typical schematic US appearance of common pathology of respective
bowel section
Fig. 14.6 Contour of different bowel partitions. (a) US appearance of normal proximal jejunum
with typical folds (uid lled). (b) Normal uid-lled ileum: no folds, no haustrae. (c) Fluid-lled
colon: haustrae can nicely be visualised
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M. Riccabona
Finally, add CDS for assessing bowel wall vasculature and main feeding vessels;
in some applications (e.g. NEC), assessment of mesenteric artery/vein and coeliac
trunk helpful.
Complete investigation by sampling relevant vessels for spectral analysis of
Doppler ow prole.
Note Modern tools helpful (harmonic imaging, high-resolution imaging, perineal
US, image compounding, graded compression, etc.). High-contrast preset advisable
(to be changed for assessing subtle alterations of wall structure).
14.2.3 Normal US Findings
Typical stratied bowel wall, “gut signature”: at least three, often ve layers depictable—echogenic supercial mucosa, hypoechoic deep muscular mucosa, echogenic
submucosa, hypoechoic muscle and echogenic serosa (Fig.14.7).
Bowel wall thickness varies with distension and age; in older children cut-off is
a thickness of 3mm for small bowel and 4mm for is colon.
Inner contour varies with segment: multiple deep folds in jejunum, less and
smaller folds in ileum and haustrae (including outer contour) in colon.
Peristalsis: regular and propulsive in small bowel, rare in colon, documented by
M-mode or video clip (Fig.14.7b).
Bowel lumen variable—depends on alimentation, gaseous content, etc., normally good compressibility.
Doppler: depends on splanchnic activation—if fasted neonatal normal value of
SMA ow in newborns=40–60cm/s. RI > 90%; then gradually changing towards
adult values within rst years of life.
Fig. 14.7 US appearance of bowel wall and peristalsis. (a) Normal bowel wall stratication seen
in non-high magnication: at least three layers recognisable (with modern high-resolution transducers even ve): hypoechoic inner “mucosa”, echogenic “submucosa” and hypoechoic muscle.
(b) M-mode used to document the intense and irregular small bowel peristalsis in a child with
gastroenteritis and thus uid-lled loops with some ascites. (c) Bauhin’s valve visualised after
saline enema
14 US oftheGastrointestinal (GI) Tract
Fig. 14.8 Saline enema—hydrocolon for small
left colon. Axial section left upper quadrant:
uid- lled narrow/small left colon (seen as
circular thin-walled structure on left upper image
corner) after saline enema; small bowel loops
distended and lled with echogenic meconium.
Some ascites
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14.2.4 Pathology
14.2.4.1 Congenital Anomalies
Most important: various forms of atresia and stenosis, position anomalies by malxation and malrotation, enteric duplications and Meckel’s diverticulum.
Usually suspected by prenatal US; postnatally often only plain lm is sufcient,
complemented by US and in some conditions uoroscopy (enema, upper GI series,
follow-through).
Atresia
Denition
Congenital occlusion or high-grade stenosis of bowel lumen.
US Findings
Proximal uid-lled distended bowel loops, sudden change in diameter at obstruction, collapsed loops in distal parts.
In high atresia (duodenum, jejunum), meconium may be present in distal parts.
In distal atresia bowel without meconium and narrow (“unused bowel”)—such a
small colon may be conspicuously visualised after saline enema (Fig.14.8).
Note In stenosis or webs with central perforation, some residual content and distension
of distal bowel loops may be present. US may show these ndings—usually not necessary. Annular pancreas difcult to prove on US, usually diagnosed intraoperatively.
• In high atresia—after plain lm with clinical symptoms—direct surgery without
further imaging performed.
• Sometimes in low atresia or equivocal ndings (e.g. stenoses/webs with partial
obstruction and annular pancreas) US or bowel follow-through requested.
Special Application: Anal Atresia
• Potential stulae and length of atretic segment assessed by perineal US applying
measurements (as in radiographs), classied as low (<1 cm), intermediate
(1–2cm) and high (>2cm) essential for planning treatment (Fig.14.9). Dynamic
assessment of defecation achievable in stenosis/for DDx Hirschsprung disease—
provided rectum can be lled with saline enema.
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M. Riccabona
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Fig. 14.9 Perineal US in anal atresia/stenosis. (a) Narrow anal canal with dilated rectum. (b)
Abnormal course and stula-like tract form rectal pouch to anal grove in intermediate anal atresia
nicely visualised by sagittal perineal scan. (c) Dotted line outlines long atretic anal canal in high
anal atresia—from anal grove (+) to rectal pouch
Note Measurements on US may differ from those on “Columbus” view radiogra-
phy (“bottom up” lateral cross-table view), as lowest rectal part/pouch may not be
sufciently lled with gas for correct radiographic depiction, or as transducer pressure may shorten distance.
• Sometimes pelvic oor muscles may be appreciated—more easily assessable by
3DUS with reconstructions, if sufcient access and resolution available.
• US enema combined with US genitography (and ce-VUS) can enable thorough
sonographic work-up of even more complex cloacal malformations (supple-
mented by uoroscopy for some queries, sometimes MRI, or very rarely ce-CT).
Malrotation
Denition
Atypical rotation/insufcient xation of gut—potentially with resulting (intermittent) obstructive symptoms. Based on incomplete foetal rotation of foregut.
US Findings
Relation of mesenteric vessels at mesenteric root—typically mesenteric vein to the
right of superior mesenteric artery (in front of aorta) (Fig.14.10).
Duodenum normally crossing retroperitoneally (behind mesenteric vessels).
Note Atypical position of mesenteric vessels not diagnostic, as rotation anomalies
may coexist with normal upper vessel position, and normal rotation may be present
in spite of inverse vessel relation.
Diagnosis of relevant malrotation: Demonstration of abnormal position of
duodeno- jejunal exure (after lling stomach/duodenum) by US or uoroscopy
(upper GI study), or following duodenal C in a normal path with the transverse duodenum crossing from right to left behind the mesenteric vessels (also easier by lling
duodenum—can be markedly enhanced by ce-US, applying diluted UCA orally).
Malposition of colon most easily seen after hydrocolon—inverse position of
descending colon, wrong position of (mobile?) coecum. Cannot be used for diagnosing malrotation.
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Fig. 14.10 Mesenteric vessels/malrotation. (a) Normal position of superior mesenteric vein (left,
in front of IVC) and artery (right, surrounded by a small collar of echogenic fat). (b, c) Inverse
position of mesenteric vessels in malrotation on grey scale (b) and CDS (c, artery on patient right/
image left side encoded in red, vein encoded in blue)
Fig. 14.11 Whirlpool sign—volvulus. (a) Grey scale appearance of volvulus: central vessel
(artery), circular swirling tissue and vascular structures. (b) CDS of same patient: whirlpool-like
spiral vessels coursing around central superior mesenteric artery more clearly depictable and convincingly obvious
Note Physiologically elongated, right-sided sigmoid loop (particularly in preterm
babies) does not indicate malrotation; normal position of colon does not exclude
small bowel malrotation.
Most important complication—volvulus.
Volvulus
Denition
Cork screw-like torsion of upper small bowel around mesenteric root, leading to
vascular compromise and bowel ischaemia/haemorrhagic infarction.
Commonly presents in rst weeks/months of life as surgical emergency.
US Findings
Prestenotic dilated, uid-lled duodenum with abrupt disruption by pseudotumourous structure, formed by clockwise twisted dilated superior mesenteric vein curling
around more centrally positioned superior mesenteric artery—whirlpool sign
(Fig.14.11). More or less echogenic mesentery and bowel.