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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
14.2.6.3 Henoch–Schönlein Purpura
Definition
Systemic vasculopathy that may affect intestines (as well as kidney and other
organs).
US and CDS Findings
Nonspecic 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 duodenum/
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 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.
14.2.6.4 Appendicitis
Definition
Inammation of appendix with risk of perforation, abscess formation, peritonitis
and stulae:
• Reactive changes often seen in many other abdominal conditions (Crohn’s dis-
ease, cystic 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: 3–6mm.
In inammation: 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.14.23).
14 US oftheGastrointestinal (GI) Tract
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Fig. 14.23 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 inamed incompressible appendix with echogenic
adjacent mesentery; wall stratication nearly lost—intraoperatively found to be phlegmonous,
almost necrotic. (f) Enlarged thick inamed 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 inamed appendix deep behind bowel loops
Painful on graded compression/sonopalpation.
Surrounding mesentery usually hyperechoic, commonly some ascites,
regional nodes.
With ongoing disease there is necrosis—wall structures get hazy, differentiation
lost, increasingly enlarged.
With perforation peri-appendiceal uid, complex collections and abscess formation (pericoecal, cul-de-sac, inammatory intestinal pseudotumour) (Fig.14.24)—
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.
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Fig. 14.24 Perforation in appendicitis. (a) Pericoecal abscess after ruptured appendicitis. (b)
Postoperative collection with oating, intraoperatively lost appendicolith—consistent with peritoneal abscess. (c) Complex cystic mass with echogenic thickened mesentery—mesenteric abscess
(originating from mesenteric lymphadenopathy)
M. Riccabona
Chronic appendicitis usually exhibits enlarged appendix with rather thin, but
structured wall, only little pain on sonopalpation, may not be very compressible:
• Potentially only little perifocal mesenteric reaction.
• Typically in chronic diseases (e.g. Yersinia, cystic brosis and intestinal obstruc-
tion syndromes).
CDS
Acute appendicitis: initially hypervascularisation of appendiceal wall with diastolic
hyperaemia on spectral analysis:
• However, may also be reactive in other inammatory bowel conditions, tachy-
cardia, systemic conditions and therefore not specic.
• 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. Henoch–
Schönlein 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 appendi-
ceal changes observed in other conditions (e.g. severe gastroenteritis).
14 US oftheGastrointestinal (GI) Tract
363
Additional Imaging
Sometimes helpful—increasingly questioned in the majority of cases for radiation
protection, as US + laboratory + clinical inspection often sufce:
• Abdominal plain 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. inamed Meckel’s diver-
ticulum, appendiceal tumour/appendiceal carcinoid).
14.2.6.5 Crohn’s Disease
Definition
Typical autoimmune condition—may manifest during (late) childhood, usually
affects small bowel, may also affect colon and can be multi-segmental:
• Ulcerating colitis (most important differential diagnosis) only affects colon
(see below).
US Finding
Thickening of bowel wall with intramural lymph nodes, reactive echogenic/
enlarged/stiff mesentery (may exhibit comb sign created by multiple vessels), commonly many enlarged lymph nodes (Fig.14.25).
Affected bowel segments incompressible/stenotic.
Often seen in terminal ileum (+ appendix), all other segments may be involved.
• Secondary affected bowel loops may form inammatory pseudotumourous con-
glomeration. In chronic stages—residual stenosis, some residual thickening,
signs of ileus, stulae tracts and abscess formation.
ab c
Fig. 14.25 Crohn’s disease. (a) Thickened wall (+ +) with stenotic bowel lumen, some preserved
wall stratication, lack of compressibility, echogenic mesenteric reaction and in patient with acute
Crohn’s disease. (b) Cross section through terminal ileum with thick wall, narrow lumen and echogenic mesenteric reaction. (c) Extended view of Crohn’s disease helps to better visualise and measure the entire extent in long affected segments. Again note reactively involved echogenic mesentery
364
ab
M. Riccabona
CDS
Impressive hypervascularity and hyperperfusion on spectral analysis (high diastolic
ow, low RI) of bowel wall in active stages (Fig.14.26).
• Used to judge activity:
– Higher resistance ow pattern with lower ow velocities indicates either
beginning necrosis or improvement under therapy, even if wall remains thick;
stenosis may persist.
– Chronic stages—no hypervascularisation. No hyperaemia.
Role of US
Essential part of initial work-up/initial diagnosis, but also for follow-up.
By lling bowel with saline enema or drinking formula (similar to those used for
MR-enteroclysis), bowel can be distended and stenotic components can be observed
on US; even stula may sometimes be visualised (Fig.14.27).
Fig. 14.26 CDS in Crohn’s disease. (a) aCDS superbly visualises hypervascularity of bowel wall
in acute Crohn’s disease. (b) CDS with spectral trace proves vascular nature of colour signals,
demonstrates low-resistance hyperaemic ow in acute phase
Fig. 14.27 Complications in Crohn’s disease: stula, stenosis. (a) Regional stenosis in acute
Crohn’s disease with thickened bowel wall (+ +) and lack of intraluminal air (which can still be
appreciated as echogenic band before and after stenosis) at most severe narrowing of bowel lumen.
(b) Fistula tract with air bubbles (arrow) indicating connection from bowel lumen to abscess pocket
14 US oftheGastrointestinal (GI) Tract
365
Complementary Imaging
MR-enteroclysis, colonoscopy.
CT enteroclysis reluctantly used in children due to radiation issues, particularly
as repeated follow-up exams would lead to unacceptably high cumulative dose.
• Fluoroscopic enteroclysis only used in selected few cases.
• Plain lm valuable in case of suspected perforation.
14.2.6.6 Colitis
Autoimmune condition, bacterial/viral, toxic or antibiotic induced, neutropenia
(after chemotherapy) or granulomatous disease—all may manifest during childhood.
Ulcerative colitis only affects colon/sigmoid, can be multi-segmental:
• DDx for Crohn’s disease: histology after colonoscopy, no small bowel involved,
slightly different US appearance (ulcers seen).
US Finding
Thickening of colon wall, potential intramural lymph nodes, reactive echogenic/
enlarged/stiff mesentery, enlarged lymph nodes possible as well as some ascites.
Disruption of inner mucosal layer by ulcerations.
Affected segments painful and less compressible or dilated, with atypical content
(Fig.14.28).
Note Usually thickening less extensive than in Crohn’s; appearance may vary with
underlying entity.
In chronic stages—residual stenosis, some residual thickening, stula tracts/
abscess formation rare.
CDS
Hypervascularity/hyperperfusion (on spectral analysis—high diastolic ow, low
RI) of bowel wall.
• Chronic stages—no hypervascularisation.
Fig. 14.28 Colitis. Enlarged lax left colon
segment with complex atypical content and
slightly thickened wall without wall destruction,
less compressible. No ulcerations seen
(Clostridium colitis)
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M. Riccabona
Role of US
Essential part of initial diagnosis, but also for follow-up.
Filling colon with saline enema (“sonographic hydrocolon”): better distension,
improved view, polyps and stenotic components better assessable.
Neonatal colitis may show similar ndings, though with smaller measurements—but US remains unspecic.
Complementary Imaging
MR-enteroclysis, colonoscopy.
14.2.6.7 Other Inflammatory Bowel Conditions
Maldigestion and malabsorption syndromes, etc. may lead to inammatory reaction
of bowel (e.g. coeliac disease, various food intolerances, granulomatous disease/
sarcoidosis).
Bowel may also be affected in many other conditions: Kawasaki disease, cystic
brosis, lymphangioectasia (“protein loosing enteropathy”—to be differentiated
from partial chronic volvulus in malrotation), chronic congestive situations (portal
hypertension), graft versus host disease, during/after chemotherapy, etc.
In chronic stages atrophy of affected bowel segments (mostly mucosa), rarefaction of folds, etc. occurs.
US Finding
Mostly/initially nonspecic ndings—as in gastroenteritis: thickening of bowel
wall (particularly mucosa), increasingly hazy differentiation of wall layers due to
oedematous changes, atypical content.
In chronic/later stage: wall narrowing, mucosa becomes atrophic, stratication
of bowel wall may be lost and folds rarefacted/small.
Reactive lymph nodes may appear, altered peristalsis often observed (transient
ileo-ileal intussusception), atypical content of bowel lumen.
Secondary ascites, pleural/pericardial effusion, haepatopathy, etc. may be noted.
Role of US
Never diagnostic—but US may give diagnostically valuable information in unclear
abdominal situations, identifying involvement of bowel in present condition—thus
directing further work-up.
14.2.6.8 Bowel Trauma
Haematoma or perforation/rupture, as well as vascular/perfusion insult.
US Finding
• Most often seen in duodenum, or ank area.
• Regional thickening of bowel wall (oedema, haematoma) with atypical appear-
ance which changes over time, from inhomogenously hyperechoic to eventually
complex hypoechoic (Fig.14.29a).
• Reactive changes of mesentery, reactive enlarged lymph nodes in later stage.
ab
14 US oftheGastrointestinal (GI) Tract
Fig. 14.29 Bowel trauma. (a) Subacute impressive bowel wall haematoma after vehicle accident.
CDS activated to document avascular nature of pseudotumourous lesion. (b) Complex free uid
behind and above bladder in subacute posttraumatic haemoperitoneum. Note sedimentations
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• Complex ascites, particularly if ruptured (Fig.14.29b).
• Free peritoneal air (see respective chapter). Secondary stenosis.
CDS
• May show reactive hypervascularity and hyperperfusion or even necrotic non-
perfused sections in vascular injury.
Role of US
US may depict indirect ndings (perfusion disturbance, free air, thickened wall,
disruption site, haematoma, etc)—not very good in ruling out any condition, particularly in early stage.
14.2.7 Mesentery
In children peritoneal cavity and slim mesentery usually not seen—only depictable
with ascites and/or if thickened/more echogenic.
14.2.7.1 Mesenteric (Peritoneal) Masses
Cyst
Easy to nd on US—usually represents simple mesenteric cyst; exhibits all features
of “simple cyst” and shows “root” at mesentery (Fig. 14.30a). May become
infected—then differentiation from other entities is difcult.
DDx Lymphatic malformation (often with secondary haemorrhage), teratoma
(wall? calcication? nodular-solid compartments?), trapped uid/old abscess,
meconium pseudocyst (typically with calcied wall), duplication cyst (gut signature
of wall), ovarian cyst (daughter cyst?), Meckel’s diverticulum, necrotic-cystic other
tumour, etc.—carefully observe additional signs such as debris and sedimentation,
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Fig. 14.30 Mesenteric cystic formations. (a) Large mesenteric cyst (+ +) in a girl, reaching from
bladder roof to liver. Size only measurable using extended view US. (b) Abdominal (mesenteric)
cystic lymphatic vascular malformation, with multiple cysts and partially sedimented echoes due
to haemorrhage
M. Riccabona
wall thickness and structure, fat or calcications, daughter cyst, relation to other
abdominal structures and vascular supply.
Lymphatic Vascular Malformation and Other Tumours
Same appearance as anywhere else in the body, may become quite large, also arise
from adjacent compartments (e.g. retroperitoneum), not to be differentiated from
other mixed mesenchymal tumours or veno-lymphatic malformation: often show
haemorrhagic cysts with sedimentation (Fig.14.30b). Rarely also arterio-venous
vascular malformations may occur (see also Fig14.36).
Rarely other tumours may occur—US may depict mass, will not allow denitive diagnosis.
DDx: mesenteric inammation and inammatory pseudotumours, mesenteric
infarction (echogenic tumour-like mass, in infarction no vascularisation, in inammation hypervascular, in abscess hyperaemic wall).
14.2.7.2 Abscesses
Relatively rare unless in appendicitis (see there).
Same appearance as everywhere else in the body.
Arise from lymph nodes (see below) or secondary to appendicitis (see above),
stulae and perforation.
US and CDS Findings
• Complex mass with complex uid in centre, some membrane-like borders in
periphery (Fig.14.31).
• Border is usually hypervascular, centre does not exhibit any vessels.
Differentiation of abscess from complex/entrapped ascites may be difcult (or
from entrapped loops with complex content):
• Sometimes only lling of bowel by enema (“US enema”, “hydrocolon”) will
enable denite separation of these entities.
• Sometimes stula tracts visualised (most commonly in Crohn’s disease, but also
in others, e.g. recurrent appendicitis).
ab
14 US oftheGastrointestinal (GI) Tract
Fig. 14.31 Abdominal/mesenteric abscess. Two examples of abdominal complex cystic pseudotumourous formations consistent with (intraperitoneal) abscesses, with a more or less dened wall
as depicted by its hypervascularisation on CDS. (a) Perforated Meckel’s diverticulum and
(b) abscess after bowel perforation
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DDx Regional haematoma, necrotic material from omental infarction/twisted
appendix epiploicae, necrotic lymph nodes, necrotic tumours.
Note In all these conditions, secondary inammatory component can never be
ruled out, even by other imaging.
Additional Imaging
CT or MR—if not obvious on US for diagnosis/DDx, sometimes (in complicated
cases) preoperatively.
14.2.7.3 Twisted Appendices Epiploica
Physiologic appendices epiploicae not depicted.
If twisted (rare in childhood)—become necrotic due to haemorrhagic infarction—sudden pain, nonspecic laboratory alterations—may pose a DDx to
appendicitis.
US Findings
Area close to bowel with increased echogenicity, sometimes hazy margin, local pain
on sonopalpation and noncompressible, some uid and mesenteric reaction, no vessels found within on CDS.
14.2.8 Mesenteric Lymph Nodes
Using graded compression technique, typical (normal sized) mesenteric nodes often
seen physiologically.
Present also in gastroenteritis, coeliac disease and other nonspecic conditions
(inammation, congestion, food intolerance, after intussusception, with tumours, etc.).