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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5795_Библиотеки_им_академика_М_И_Перельмана.pdf
350
M. Riccabona
Depending on severity and duration: peritoneal uid, thickened echogenic bowel
wall with haemorrhage and oedema.
Note US diagnostic, once whirlpool sign seen—do not waste time with further
imaging. In equivocal situations emergency uoroscopy should be performed to
establish the diagnosis. US less reliable for ruling out (partial, intermittent, chronic)
volvulus/malrotation—only if course of duodenum and position of duodeno- jejunal
junction clearly visible US diagnostically valid (see above).
Hirschsprung Disease/Neuronal Intestinal Dysplasia (NID)
Denition
Lack of colonic ganglion innervation with consequent lack of peristalsis, leading to
constipation and dilatation; length of aganglionic segment varies.
NID: milder innervation anomaly of colon—some transition in preterms due to
immaturity.
US Findings
Impressive dilatation of stool-lled colon (megacolon) (Fig.14.12), coprolith (also with
other severe constipation); sometimes transition zone with change in calibre depictable.
• US enema improves depiction of and assessment of length of affected segment.
• Complete investigation by perineal access.
Note The aganglionic segment may be difcult to depict, very short segments or
very long segments may be missed (latter misinterpreted for chronic constipation).
Diagnosis made by suction biopsy/histology; often manometry/defecography
performed preoperatively.
Duplication/Diverticula
Denition
Double lumen with or without connection—wide connection may cause difculties
in differentiating real enteric duplication from diverticula.
DDx: any other abdominal cyst (mesenteric/ovarian cyst, meconium pseudocyst, pancreas pseudocyst), ascites, seroma, Meckel’s diverticulum, cystic
Fig. 14.12 Hirschsprung and constipation. (a) Dilated colon with echogenic content in infant
with Hirschsprung. Some ascites. (b) Child with severe constipation: very echogenic colon content
with shadowing—consistent with huge coprolith (similar appearance seen with bezoars)
14 US oftheGastrointestinal (GI) Tract
Fig. 14.13 Bowel duplication. (a) Bowel duplication cyst—cystic structure with thick wall that
exhibits bowel stratication (“gut signature”). (b) Child with gastric duplication cyst: uid-lled
structure adjacent to stomach at pre-pyloric area with bowel wall appearance, moves with stomach
during peristalsis. (c) Large simple cyst with thick multilayered wall adjacent to uid-lled duodenal loop coursing below which is compressed by the duplication cyst explaining the clinical symptoms of intermittent upper obstruction
351
abc
Fig. 14.14 Dynamic US after drinking tea for lling a duplication cyst. (a) Some uid within a
typical duplication cyst that could easily be mistaken for a uid-lled atypical bowel loop or stomach. (b) After drinking tea cyst starts to ll and enlarge. (c) Increasing dilatation some time after
drinking tea, proving connection of cyst with bowel lumen and also explaining the intermittent
nature of the patients’ obstructive symptoms
lymphatic malformation/teratoma, covert perforation, etc.—often differentiation
achievable by typical US features of enteric duplication’s wall structure.
US Findings
Most common in stomach, duodenum and colon. Oesophageal/small bowel duplications less common.
• Exhibit thick wall around cyst with typical gut wall structure (“gut signature”)
(Fig.14.13).
• Usually adherent to adjacent (potentially compressed) bowel loop with common
vascular supply.
• Move concordant to intestinal peristalsis of respective bowel loop.
• May have sedimented internal echoes.
• If connection between duplication and bowel lumen, size may vary depending on
bowel content and lling—use peroral or rectal lling by tea/formula/saline
enema to enable diagnosis, air content possible (Fig.14.14).
352
Fig. 14.15 Meckel’s diverticulum. Axial section, right
lower quadrant—typical US image of Meckel’s
diverticulum: thick wall, some complex uid content,
adjacent to coecum
M. Riccabona
Note Solid duplications with only minimal lumen rare, more difcult to depict.
Meckel’s Diverticulum
Denition
Remnant of omphalo-enteric duct. May present as acute abdomen (query appendicitis), particularly after haemorrhage.
US Findings
Cyst-like formation with gut-like thick wall (Fig.14.15). Size may vary; shape/
content depends on size, potential haemorrhage (from ectopic gastric mucosa) and
potential connection to bowel lumen—otherwise similar to duplication cyst, only
common wall much thicker.
• Typically located right lower quadrant or situated along omphalo-enteric
duct tract.
• Commonly does not change position with bowel peristalsis, not compressible.
Note US not always 100% decisive. If necessary for treatment decision—Meckel’s
scintigraphy/laparoscopy. If equivocal and no surgery planned—additional imaging
(sectional? uoroscopic?).
14.2.5 Acquired Obstructive Pathology
14.2.5.1 Meconium Ileus
Definition
Obstruction by inspissated meconium, commonly seen in preterm infants, after
dehydration, or associated with cystic brosis.
ab
14 US oftheGastrointestinal (GI) Tract
Fig. 14.16 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: uid- 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 lled with echogenic meconium and some ascites
353
US Findings
Dilated small bowel loops with very echogenic content, typical for meconium
(Fig.14.16).
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 calcications along peritoneum, even descending into scrotum) and meconium pseudocysts (appear as complicated cyst, potentially
calcication 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 contrast
material may be added to improve results + enable post-procedure plain lm for
documentation.
14.2.5.2 Midgut Volvulus
See above.
14.2.5.3 Sigma Volvulus
May occur in children, no indication for US.
No specic ndings, except for demonstration of course of sigmoid after therapeutic saline enema.
14.2.5.4 Hernia
Definition
Herniation of abdominal content to atypical location causing transport problems,
kinks, vascular compromise and mechanic obstruction.
354
M. Riccabona
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.
Note Internal hernias usually not depicted, but indirect signs hint towards mechan-
ical 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/scrotum/labia, enlarged entrance to inguinal canal (Fig.14.17):
• Content varies (mesentery, ascites, bowel—rarely also bladder or ovary).
• Provocation manoeuvres help depicting intermittent herniation.
Diaphragmatic hernia: see chest chapter.
a
b
cd
Fig. 14.17 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
14 US oftheGastrointestinal (GI) Tract
355
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 (intraperito-
neal) content.
14.2.5.5 Intussusception
Parts of more proximal bowel (intussusceptum) slip into more distal parts
(intussuscipiens):
• Small bowel intussusception: commonly happens in many conditions in the jeju-
num/ileum (gastroenteritis, hyperperistalsis, hyperreactive bowel, etc.)—sponta-
neously resolve unless there is a pathologic lead point (diverticula, large lymph
node, etc.). Diameter usually <2cm (Fig.14.18).
• Ileo-colic intussusception/invagination: less common, but most important (emer-
gency condition!)—associated with gastroenteritis, mesenteric adenopathy and
mobile coecum. Long-standing intussusception causes venous congestion, even-
tually ischaemic damage and bowel necrosis with perforation. Compromised
vascular supply in the mesentery also pulled into intussusception and com-
pressed, 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
ndings (DDx, atypical lead points, etc.).
Fig. 14.18 Transient small bowel
intussusception. Target sign in left upper
quadrant, diameter 1.5cm, spontaneously
resolved during US investigation, in child with
hyperperistalsis and gastroenteritis—typical
appearance of transient small bowel
intussusception
356
Fig. 14.19 Ileo-colic intussusception. (a) Axial section: typical doughnut sign in ileo-coecal
intussusception, 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 uid. (c) Some adjacent uid in this intussusception which already has reached
into descending colon—visible from left ank. (d) Hydrostatic reduction of intussusception: uid
from enema in intussuscipiens starts to surround and mobilise intussusceptum. (e) Axial section
lower right quadrant: after hydrostatic reduction coecum lled with uid, intussusception has been
reduced, ileo-coecal (Bauhin’s) valve leafs still swollen
M. Riccabona
• “Bowel in bowel” appearance; if ileocolonic—additionally entrapped hyper-
echoic 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.14.19).
• Reactive changes—ascites, mesenteric oedema and mesenteric nodes.
• Entrapped uid at head of intussusceptum, restricted/absent perfusion—sign for
poor reducibility and higher complication risk, potentially pathologic lead struc-
tures (Meckel’s diverticula, lymphoma, bowel wall tumour, polyp, etc.).
Note Always follow entire colon to coecum; intussusception usually encountered
in right upper quadrant (coecum mobile); intussusceptum can extend to rectum, or
even prolapse. If equivocal US ndings: use sonographic saline enema or conventional uoroscopic technique. Same technique with higher lling pressure used for
US-guided hydrostatic reduction (Fig.14.19d, e).
14.2.5.6 Masses andTumours
Rare. May originate from polyps (familial). Rhabdomyosarcoma and adenocarcinoma (in familial conditions) extremely rare.
Polyps more common:
14 US oftheGastrointestinal (GI) Tract
357
a b
c
de
Fig. 14.20 Gastrointestinal masses and tumours: Typical US appearance of a colonic polyp (+ …
+) after some saline enema to reduce bowel gas (a) with typical vascular supply on CDS (b). (c)
Large bowel tumour causing intussusception—proven to be a nodular type lymphoma. (d)
Inltrated and thickened bowel wall with destroyed stratication in Burkitt lymphoma. (e)
(Complex) ascites and peritoneal metastasis (+ +)—in this case from rare familiar childhood adenocarcinoma of the sigmoid: stenosis better depictable after saline enema.
US and CDS Findings
Polyps better depictable after lling bowel.
CDS helps by depicting classical vascular supply (Fig.14.20a, b).
Otherwise no difference from any other tumour—do not exhibit any specic
features (Fig.14.20c–e).
Depending on involvement/stage: local mesenteric nodes, ascites, stenosis, peritoneal/mesenteric nodes and liver metastasis.
Diagnosis by histology, staging by standard sectional imaging mandatory in
malignant conditions.
14.2.6 Inflammatory Conditions
14.2.6.1 Necrotising Enterocolitis (NEC)
Definition
Severe inammatory bowel disease of preterm and newborn babies, potentially
lethal due to necrosis and peritonitis, in late stages only surgically manageable.
358
bc
M. Riccabona
US Findings
Initially nonspecic thickened, hazy structured bowel wall, often echogenic content, hypervascularisation, ascites (Fig.14.21a, 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.14.21c, d and 14.22). Enlarged
nodes rare; abscess formations may occur.
Calcied peritoneal content indicates old (foetal) perforation with meconium
peritonitis.
In perforation free air detectable by meticulous scanning—see respective entry.
CDS Findings
Initially hyperaemia of mesenteric arteries (increased 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.14.21e).
Portal venous gas bubbles seen as typical spikes on spectral ow pattern—difcult to visualise in main portal vein on CDS, but reverberation echoes and twinklinglike artefacts seen within liver periphery (Fig.14.22).
Systolic velocity >100 cm/s and RI < 0.80 (coeliac trunk/mesenteric artery)
highly suspicious for inammatory condition—provided patient is fasted.
a
de
Fig. 14.21 NEC. (a) Early phase of NEC: atypical bowel wall, dilatation (similar to plain rm
ndings in the early stage) and some ascites. (b) CDS reveals inammatory 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 bubbles in NEC with pneumatosis. (e) Thickened bowel wall with destroyed stratication, no depictable vasculature—necrotic segment
abcd
14 US oftheGastrointestinal (GI) Tract
Fig. 14.22 Portal venous/liver gas. (a) CDS with spectral trace of portal vein: on CDS normal
ow direction displayed, whereas spectral analysis additionally demonstrates short 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 ow
359
Role of US
Increasingly important.
Very sensitive to early changes before plain lm shows typical pathology.
However, specicity of 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, hypertrophic pyloric stenosis,
oncology—atrophic mucosa...).
DDx of intrahepatic portal venous gas—peripheral intrabiliary air/gas.
Additional Imaging
Abdominal plain lm, laboratory.
14.2.6.2 Gastroenteritis
Not an indication for US—however, ndings often encountered during US for
unclear abdominal complaints, appendicitis, etc.
US and CDS Findings
Atypical bowel content, often complex uid.
Hyperperistalsis, mesenteric changes (increased echogenicity, mesenteric lymph
nodes) and some ascites.
Nonspecic bowel wall changes, no specic features.
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.