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Fig. 9.14 Dynamic US after drinking tea for fi lling a duplication cyst. ( a ) Some fl uid within a
typical duplication cyst that could easily be mistaken for a fl uid-fi lled atypical bowel loop or stom­ach. ( b ) After drinking tea cyst starts to fi ll and enlarge. ( c ) Increasing dilatation some time after drinking tea, proving connection oft cyst with bowel lumen and also explaining the intermittent nature of the patients’ obstructive symptoms
9 US of the Gastrointestinal (GI) Tract
Fig. 9.15 Meckel’s diverticulum. Axial section, right lower quadrant – typical US image of
Meckel’s diverticulum: thick wall, some complex fl uid content, adjacent to coecum
NOTE : US not always 100 % decisive. If necessary for treatment decision – Meckel’s scintigraphy/laparoscopy. If equivocal and no surgery planned – addi­tional imaging (sectional? fl uoroscopic?).

9.2.5 Acquired Obstructive Pathology

9.2.5.1 Meconium Ileus
Defi nition
• Obstruction by inspissated meconium, commonly seen in preterm infants, after dehydration, or associated with cystic fi brosis.
US Findings
• Dilated small bowel loops with very echogenic content, typical for meconium (Fig. 9.16 ).
9.2 Bowel
a b
Fig. 9.16 Meconium ileus. ( a ) Dilated small bowel loop with echogenic content and some ascites
in preterm with meconium transport problems; note collapsed bowel loop more distal. ( b ) Same baby as in ( b ), during saline enema for DDx (e.g. atresia) and reduction of meconium ileus: fl uid- fi lled narrow colon (“small left colon”), tip of thin feeding tube for enema positioned in descending colon seen at right upper corner, dilated small bowel loop fi lled with echogenic meconium and some ascites
• Abrupt calibre change from dilated to very narrow bowel.
• Improved: depiction of transition zone to nonused bowel by saline enema.
• Secondary perforation with formation of complicated ascites/meconium perito­nitis (typically develop calcifi cations along peritoneum, even descending into
calcifi cation in cyst wall).
NOTE : Repeated bedside saline enema under US guidance may be used for relief of meconium ileus (see also Fig. 2.1 ). Acetylcysteine or isotonic radiopaque con- trast material may be added to improve results + enable post-procedure plain fi lm for documentation.
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9.2.5.2 Midgut Volvulus
See above.
9.2.5.3 Sigma Volvulus
May occur in children, no indication for US.
No specifi c fi ndings, except for demonstration of course of sigmoid after thera-
peutic saline enema.
9.2.5.4 Hernia
Defi nition Herniation of abdominal content to atypical location causing transport problems, kinks, vascular compromise and mechanic obstruction. Causes Adhesions of various origin, atypical peritoneal bands (related to internal hernias) or remnant/reoccurrence of pathologic openings of peritoneal cavity to other loca­tions (inguinal, diaphragmatic, Ladd’s bands, abdominal wall, etc.). US Findings (and Role) To depict and assess herniation if area accessible for US.
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9 US of the Gastrointestinal (GI) Tract
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Fig. 9.17 Inguinal hernia. ( a ) Seen in longitudinal section of inguinal canal and scrotum. ( b )
Slight gapping of inner opening of inguinal canal (+ +), bowel just starts to enter into hernia (lon­gitudinal section paramedian at inguinal area). ( c ) Inguinal hernia, longitudinal section: course of canal seen with some mesentery entering into hernia. No typical testis seen. ( d ) Inguinal hernia with unusual content in infant girl: obviously ovary entrapped in inguinal canal. CDS activated (low-velocity scale settings used, accepting aliasing) to prove existing ovarian perfusion
NOTE: Internal hernias usually not depicted, but indirect signs hint towards mechanical obstruction (e.g. dilated bowel loops, thickening of bowel wall, marked difference of bowel lumen size between proximal and distal loops and yo-yo hyperperistalsis). Inguinal hernia : demonstration of abdominal content within inguinal canal/scro- tum/labia, enlarged entrance to inguinal canal (Fig. 9.17 ):
• Content varies (mesentery, ascites, bowel – rarely also bladder or ovary).
• Provocation manoeuvres help depicting intermittent herniation. Diaphragmatic hernia : see chest chapter. Abdominal wall hernia : same rules apply as for inguinal hernia, may also occur
postoperatively in scars. DDx :
• Clinically any other cause of obstruction causing mechanical obstruction or mimicking herniation.
• In boys consider funiculocele, in preterms physiological weakness of inguinal canal with physiologically persisting continuity that resolves spontaneously.
NOTE : US may not rule out all defects, only demonstrates herniation of (intraperi- toneal) content.
9.2.5.5 Intussusception
Parts of more proximal bowel (intussusceptum) slip into more distal parts (intussuscipiens):
9.2 Bowel
Fig. 9.18 Transient small bowel intussusception. Target sign in left upper quadrant, diameter
1.5 cm, spontaneously resolved during US investigation, in child with hyperperistalsis and
gastroenteritis – typical appearance of transient small bowel intussusception
• Small bowel intussusception: commonly happens in many conditions in the jeju­num/ileum (gastroenteritis, hyperperistalsis, hyperreactive bowel, etc.) – sponta­neously resolve unless there is a pathologic lead point (diverticula, large lymph node, etc.). Diameter usually <2 cm (Fig. 9.18 ).
• Ileo-colic intussusception/invagination: less common, but most important (emer­gency condition!) – associated with gastroenteritis, mesenteric adenopathy and mobile coecum. Long-standing intussusception causes venous congestion, even­tually ischemic damage and bowel necrosis with perforation. Compromised vas­cular supply in the mesentery also pulled into intussusception and compressed, rarely resolves spontaneously.
• Colo-colonic intussusception: much rarer, usually happens only with underlying pathologic conditions (e.g. polyps).
US and CDS Findings
• US – mainstay of diagnosis, can reliably diagnose (and most often exclude) intussusception in skilled hands; also used for follow-up after reduction/to see alternate fi ndings (DDx, atypical lead points, etc.).
• “Bowel in bowel” appearance; if ileocolonic – additionally entrapped hyper­echoic mesentery with respective vessels, often lymph nodes. Bowel wall may be thick and oedematous. “Pseudo-kidney sign” (longitudinal section) or “doughnut sign” (axial section) (Fig. 9.19 ).
• Reactive changes – ascites, mesenteric oedema and mesenteric nodes.
• Entrapped fl uid at head of intussusceptum, restricted/absent perfusion – sign for poor reducibility and higher complication risk, potentially pathologic lead struc­tures (Meckel’s diverticula, lymphoma, bowel wall tumour, polyp etc.).
NOTE : Always follow entire colon to coecum; intussusception usually encoun- tered in right upper quadrant (coecum mobile); intussusceptum can extend to rectum, or even prolapse.
• If equivocal US fi ndings: use sonographic saline enema or conventional fl uoro­scopic technique.
• Same technique with higher fi lling pressure used for US-guided hydrostatic reduction (Fig. 9.19d, e , also see Fig. 2.3 ).
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Fig. 9.19 Ileo-colic intussusception. ( a ) Axial section: typical doughnut sign in ileo-coecal intus-
susception, with centrally some echogenic mesentery supplying inner small bowel loop (intussus­ceptum). ( b ) Longitudinal view: pseudo-kidney sign created by inner and outer loop. Some entrapped fl uid. ( c ) Some adjacent fl uid in this intussusception which already has reached into descending colon – visible from left fl ank. ( d ) Hydrostatic reduction of intussusception: fl uid from enema in intussuscipiens starts to surround and mobilise intussusceptum. ( e ) Axial section lower right quadrant: after hydrostatic reduction coecum fi lled with fl uid, intussusception has been reduced, ileo-coecal (Bauhin’s) valve leafs still swollen
9.2.5.6 Tumours
Rare. May originate from polyps (familial). Rhabdomyosarcoma and adenocarci­noma (in familial conditions) extremely rare. US and CDS Findings
• No difference from any other tumour.
• Do not exhibit any specifi c features (Fig. 9.20 ). Depending on involvement/stage: local mesenteric nodes, ascites, stenosis, peri-
toneal/mesenteric nodes and liver metastasis.
Diagnosis by histology, staging by standard sectional imaging mandatory in
malignant conditions.

9.2.6 Inflammatory Conditions

9.2.6.1 Necrotising Enterocolitis (NEC)
Defi nition
• Severe infl ammatory bowel disease of preterm and newborn babies, poten­tially lethal due to necrosis and peritonitis, in late stages only surgically manageable.
9.2 Bowel
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Fig. 9.20 Gatrointestinal tumours. ( a ) Large bowel tumour causing intussusception – proven to be a
nodular type lymphoma. ( b ) Infi ltrated and thickened bowel wall with destroyed stratifi cation in Burkitt lymphoma. ( c ) (Complex) ascites and peritoneal metastasis (+ +) – in this case from rare familiar child- hood adenocarcinoma of the sigmoid: stenosis better depictable after saline enema.
US Findings
• Initially nonspecifi c thickened, hazy structured bowel wall, often echogenic con­tent, hypervascularisation, ascites (Fig. 9.21a, b ).
• In later stages intramural air bubbles – seen as echogenic foci within wall (“pneu­matosis”), secondarily gas bubbles passing through portal vein into liver, accu­mulating in liver periphery (see chapter liver) (Figs. 9.21c, d and 9.22 , see also Fig. 7.17 ). Enlarged nodes rare; abscess formations may occur.
• Calcifi ed peritoneal content indicates old (fetal) perforation with meconium peritonitis.
• In perforation free air detectable by meticulous scanning – see respective entry.
CDS Findings
• Initially hyperaemia of mesenteric arteries (increased fl ow velocities, decreased RI – seen in superior mesenteric artery and celiac trunk). The longer the disease, the higher the resistance/RI values. Eventually in necrosis completely unstruc­tured segments of devascularised bowel (Fig. 9.21e ).
• Portal venous gas bubbles seen as typical spikes on spectral fl ow pattern – diffi ­cult to visualise in main portal vein on CDS, but reverberation echoes and twin­kling like artefacts seen within liver periphery (Fig. 7.22 , see also Fig. 7.17 ).
• Systolic velocity >100 cm/s and RI < .80 (coeliac trunk/mesenteric artery) highly suspicious for infl ammatory condition – provided patient is fasted.
Role of US
• Increasingly important.
• Very sensitive to early changes before plain fi lm shows typical pathology.
• However, specifi city of fi ndings low, unless intramural air/portal venous gas seen.
NOTE : Intramural air/portal venous gas rarely also seen with other conditions (e.g. idiopathic, severely dilating bowel obstruction).
• DDx of intrahepatic portal venous gas – peripheral intrabiliary air/gas.
Additional Imaging
Abdominal plain fi lm, laboratory.
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Fig. 9.21 NEC. ( a ) Early phase of NEC: atypical bowel wall, dilatation (similar to plain fi rm fi nd-
ings in the early stage) and some ascites. ( b ) CDS reveals infl ammatory hypervascularisation in now thickened bowel wall. ( c ) Small echogenic foci ( arrow ) in thickened bowel wall consistent with pneumatosis. ( d ) CDS shows reverberations (like “twinkling sign”) from intramural gas bub- bles in NEC with pneumatosis. ( e ) Thickened bowel wall with destroyed stratifi cation, no depict- able vasculature – necrotic segment
abcd
Fig. 9.22 Portal venous/liver gas. ( a ) CDS with spectral trace of portal vein: on CDS normal fl ow
direction displayed, whereas spectral analysis additionally demonstrates short fl ow spikes typical for passing gas bubbles. ( b , c ) Echogenic intrahepatic foci – portal venous or intrabiliary gas bubbles in minor and more central distribution ( b , more likely to represent biliary gas) and severe extent ( c , more likely to be portal venous gas, particularly as it accumulates in periphery). ( d ) Spectral analysis mandatory to prove intravascular nature of gas bubbles – enabling differentiating of intravascular from intrabiliary gas by depicting typical gas spikes in portal venous fl o w
9.2.6.2 Gastroenteritis
Not an indication for US – however, fi ndings often encountered during US for unclear abdominal complaints, appendicitis, etc. US and CDS Findings
• Atypical bowel content, often complex fl uid.
• Hyperperistalsis, mesenteric changes (increased echogenicity, mesenteric lymph nodes) and some ascites.
• Nonspecifi c bowel wall changes, no specifi c features.
9.2 Bowel
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• If toxic paralytic component: bowel may get dilated/lose peristalsis.
NOTE : Often self-limiting, spontaneously resolving ileo-ileal/jejunal intussuscep- tions can be observed.
• Hyperperfusion of mesenteric artery with hypervascular bowel wall.
9.2.6.3 Henoch-Schönlein Purpura
Defi nition Systemic vasculopathy that may affect intestines (as well as kidney and other organs). US and CDS Findings
• Nonspecifi c image with echogenic, thickened bowel wall (particularly mucosa).
• Lumen may have echogenic content due to haemorrhage, hypervascularisation.
• Reactive mesenteric hyperechogenicity/thickening, some ascites. Adenopathy rare.
NOTE : Bowel wall thickening due to intramural haematoma (typically at duode- num/proximal jejunum) rarely associated with bloody stools (more likely in bleed­ing diathesis) very uncommon, only after trauma or with NAI. Role of US
• Diagnosis usually made by laboratory and clinical fi ndings.
• Helpful for depiction of similar changes in bowel segments other than appendix – helps to reduce rate of unnecessary surgery, improves DDx.
• Follow up possible but usually not necessary.
• US used in protracted/complicated course with higher rate of complications (such as intussusception) or with worsening of symptoms.
9.2.6.4 Appendicitis
Defi nition Infl ammation of appendix with risk of perforation, abscess formation, peritonitis and fi stulae:
• Reactive changes often seen in many other abdominal conditions (Crohn’s dis­ease, cystic fi brosis, gastroenteritis, Henoch-Schönlein purpura, etc.) - may mimic appendicitis.
US Findings Typically located in right lower quadrant, can commonly be found when actively searching area around coecal pole (remember abnormal position such as retrocoe­cally, also look to lower margin of liver, behind/in front of ascending colon, medio­cranially, etc.).
• Normal appearance of appendix: blind ending tubular structure with typical gut wall appearance, commonly without content, compressible and painless on US palpation Diameter in children: 3–6 mm.
• In infl ammation: appendix enlarged, enhanced wall structure, may show mural follicles (follicular appendicitis) and may show content in lumen – particularly appendicolith (with distal shadowing), stiff/uncompressible (Fig. 9.23 ).
• Painful on graded compression/sono-palpation.
• Surrounding mesentery usually hyperechoic, commonly some ascites, regional nodes.
• With ongoing disease there is necrosis – wall structures get hazy, differentiation lost, increasingly enlarged.
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9 US of the Gastrointestinal (GI) Tract
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Fig. 9.23 Appendicitis. ( a ) Normal appendix in right lower quadrant, nicely depictable due to
ascites. ( b ) Thick incompressible appendix (+ +) in typical position adjacent to pelvic vessels. ( c ) CDS exhibits vivid hypervascularisation in acute appendicitis (same patient as in b ). ( d ) Typical target sign of enlarged, incompressible appendix (+ +) with thickened wall and perifocal mesen­teric reaction. ( e ) Cross section of enlarged and infl amed incompressible appendix with echogenic adjacent mesentery; wall stratifi cation nearly lost – intraoperatively found to be phlegmonous, almost necrotic. ( f ) Enlarged thick infl amed appendix with mesenteric reaction and appendicolith ( shadow ). ( g ) Thickened echogenic mucosa of swollen enlarged appendix in Henoch-Schönlein purpura. ( h ) Retrocoecal appendicitis – typical target sign of thickened, stiff and infl amed appen- dix deep behind bowel loops
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• With perforation peri-appendiceal fl uid, complex collections and abscess forma­tion (pericoecal, cul-de-sac, infl ammatory intestinal pseudotumour) (Fig. 9.24 ) – may be distributed to other parts of peritoneal cavity and thus missed.
• Floating appendicolith may enable diagnosis of abscess origin.
• After perforation appendix may be normal sized as content evacuated.
• Chronic appendicitis usually exhibits enlarged appendix with rather thin, but structured wall, only little pain on sono-palpation, may not be very compressible:
• Potentially only little perifocal mesenteric reaction.
• Typically in chronic diseases (e.g. Yersinia, cystic fi brosis and intestinal obstruc­tion syndromes).
9.2 Bowel
ab c
Fig. 9.24 Perforation in appendicitis. ( a ) Pericoecal abscess after ruptured appendicitis. ( b )
Postoperative collection with fl oating, intraoperatively lost appendicolith – consistent with perito­neal abscess. ( c ) Complex cystic mass with echogenic thickened mesentery – mesenteric abscess (originating from mesenteric lymphadenopathy)
CDS Acute appendicitis: initially hypervascularisation of appendiceal wall with diastolic hyperaemia on spectral analysis:
• However, may also be reactive in other infl ammatory bowel conditions, tachy­cardia, systemic conditions and therefore not specifi c.
• In late/gangraenous stages vascularity reduced, even lacking.
• Chronic appendicitis: usually no hyperaemia.
NOTE : In appendicitis changes often restricted to/focused on appendix. If several changes observed in other bowel segments – consider other entities (e.g. Henoch­Schönlein purpura and Crohn’s disease). Role of US Increasingly promoted, used in initial assessment of clinically unclear abdomen, particularly in girls, to different tubarian/ovarian pathology, urinary tract causes for underlying symptoms:
• However, early stages of acute appendicitis may appear sonographically normal, perforated old/subacute appendicitis may even be missed and reactive appendi­ceal changes observed in other conditions (e.g. severe gastroenteritis).
Additional Imaging Sometimes helpful – increasingly questioned in the majority of cases for radiation protection, as US + laboratory + clinical inspection often suffi ce:
• Abdominal plain fi lm: for depiction of appendicoliths/free peritoneal air in perforation.
• Emergency CT (if MRI not available) – unclear cases with pending decision on surgery (e.g. obesity hindering US assessment).
• Elective MR (if available), particularly for DDx (e.g. infl amed Meckel’s diver­ticulum, appendiceal tumour/appendiceal carcinoid).
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9.2.6.5 Crohn’s Disease
Defi nition Typical autoimmune condition – may manifest during (late) childhood, usually effects small bowel, may also affect colon and can be multi-segmental: