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Differential-Diagnosis-in-Ultrasound-Imaging.pdf
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7

Gastrointestinal Tract

Extended Wall Changes

Tract

 

 

 

 

 

Stomach

 

Enteritis

 

 

 

 

 

 

 

 

 

 

Small/Large Intestine

 

Celiac Disease (Sprue)

 

 

 

 

Gastrointestinal

 

 

Focal Wall Changes

 

Crohn Disease

 

 

Extended Wall Changes

 

 

 

 

Ulcerative Colitis

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Dilated Lumen

 

 

 

 

 

 

 

 

 

Amyloidosis

 

 

 

 

 

 

 

Narrowed Lumen

 

 

 

 

 

 

 

 

 

Pseudomembranous Enterocolitis

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Ischemia

 

 

 

 

 

 

 

 

 

Hypertrophy

 

 

 

 

 

 

 

 

 

Tumor

 

 

 

 

 

 

 

 

 

Lymphoma

Extended changes in the jejunal, ileal, and co-

ischemic, invasive, and functional causes are

lonic wall are primarily due to acute infection

much less common. Differential diagnosis has

or chronic inflammation, while toxic, allergic,

to rule out extended malignant wall changes.

Enteritis

The continuous, extended edematous thickening of the mucosa in enteritis is seen primarily in the ileum but also in the jejunum and colon. There is markedly accentuated wall layering, with the mucosa and/or submucosa being particularly thick, resulting in a narrowed lumen of the bowel. In acute enteritis the intestinal lumen always contains some fluid, even in the fasting state, and this finding is present even before the clinical symptom of diarrhea (Figs. 7.55, 7.56, 7.57, 7.58).

In the small intestine the circular folds may be pronounced, while in the colon the haustra and folds may intertwine in gyrose fashion. One characteristic sign in the small bowel is

vigorous peristalsis that propagates in an orderly antegrade way and does not exhibit any tendency to pendulate. In acute enteritis the colon, too, will demonstrate peristaltic activity. Color flow Doppler scanning may visualize inflammatory hypervascularity in the intestinal wall that, at least in its initial stages, seems to correlate with the severity of the inflammation. Outside the bowel, ascites may be present, signifying the inflammatory peritoneal reaction, as well as enlarged mesenteric lymphadenopathy.

In severe necrotizing inflammation the peristaltic activity and the inflammatory hypervascularity will subside again. There will be diffuse

tenderness along the diseased bowel segment, and the intestinal wall will be characterized by indistinct wall layering; the appearance of gas bubbles has to be regarded as a particularly ominous sign. These gas bubbles will be carried along the venous system of the mesentery and are the cause of portovenous gas embolism in the liver.

Fig. 7.55 Enteritis.

b Mesenteric lymph node enlargement.

Fig. 7.56 Non-specific enteritis.

a Enteritic small bowel.

 

 

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7

Small/Large Intestine

Fig. 7.57 Enteritis with demonstration of thickened wall, small amount of free peritoneal fluid collection (sympathic peritoneal irritation), inflammatory thickening of the lateral peritoneum.

Fig. 7.58 Enteritis in the case of a collagenosis/vasculitis.

b Severe hypervascularization.

a Edematous rigid lumen, accentuated wall layering.

 

Celiac Disease (Sprue)

Being a special case of enteric reaction, celiac disease is characterized by edema with hypoechoic thickening of the intestinal wall and marked distension of the fluid-filled lumen. The hyperperistaltic loops of the small bowel twine around each other, giving rise to the term “tumbler phenomenon” (Fig. 7.59).

Fig. 7.59 Celiac disease (sprue).

a Longitudinal scan in the midabdomen.

Crohn Disease

Crohn disease is a chronic inflammatory bowel disease occurring anywhere in the GI tract, with discontinuous extended involvement of individual bowel segments, the primary location being the terminal ileum and colon. In addition to the segmental pattern of the typical pathological changes demonstrated by ultrasound, the type and severity of the most frequent transmural inflammation and its complications, with their wildly mixed and constantly alternating pattern, are characteristic of Crohn disease (Fig. 7.60, 7.3).

Types of wall change. In Crohn disease various types of change in the intestinal wall can be seen, depending on the transmural severity of the inflammation.

On one hand, the layering of the wall becomes more pronounced and thickened, the intestinal lumen is narrowed, and, because of the impaired peristalsis (inflammatory rigidity), the segment involved may act as functional stenosis.

On the other hand, the intestinal wall may display a complete loss of normal layering, and diffuse and irregular hypoechoic thick-

b Transverse scan in the midabdomen.

ening or hyperechoic widening, which may also result in aperistaltic narrowing of the lumen.

There is a gradual transition from one type of wall change to the other.

Complications. Complications of Crohn disease can be expected to arise from the functional and/or organic stenosis (colicky pain upstream of the stenotic segment, signs of mechanical ileus in the proximal bowel loops) as well as the local inflammation. Apart from local

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7

Gastrointestinal Tract

7.3 Crohn Disease

a and b Crohn disease, accentuated wall of the terminal ileum.

c Accentuated layering of the intestinal

d Terminal ileitis (Crohn disease) with a

 

wall in the terminal ileum in Crohn disease

hazy, thickened wall (pathologic gut

 

and prevailing thickening of the submu-

sign), starting loss of layering and marked

 

cous membrane; demonstration of an ul-

panniculitis. Lymph node enlargement.

 

cer (arrow).

 

e Crohn disease; distinct destruction of the wall layering of the terminal ileum.

f Cobblestone relief of the terminal ileum in Crohn disease; posterior hyperechoic mesenteritis and enlarged lymph nodes.

g Crohn disease with inflammatory stenosis (cobblestone relief) of the lumen and dilatation of the preceding bowel loop.

h and i Terminal ileitis with inflammatory hypervascularity.

h Longitudinal scan.

i Transverse scan.

j and k Intussusception, short segment in Crohn disease.

m Crohn disease with interenteric fistula. n and o Conglomerate in Crohn disease.

l Ileocolic junction in advanced Crohn disease: stenosis in the region of the terminal ileum.

p Crohn disease with interenteric fistula.

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7.3 Crohn Disease (Continued)

q Fistula in Crohn disease.

r Duodenal Crohn disease: pathologic ac-

s Crohn colitis: pathological target sign of

 

centuated target sign and distinct panni-

the rectum posterior to the bladder with

 

culitis.

distinct panniculitis.

tenderness, color flow Doppler scanning will

Fig. 7.60 Enteritis in Crohn disease.

 

reveal inflammatory hypervascularity in the

 

intestinal wall and its vicinity. There will be

 

hyperechoic panniculitis and inflammatory re-

 

action of the greater omentum (hyperechoic

 

halo) as well as complications such as forma-

 

tion of abscesses, fistulas, and conglomerates

 

containing several loops of bowel.

 

Sensitivity and specificity are reported to be

 

90.3% and 95% respectively in the diagnosis of

 

inflammatory bowel disease,1,2 100% and 91%

 

in detecting strictures, and 87% and 90% in the

 

diagnosis of fistulas, with a bowel wall thicken-

 

ing of at least 3 mm.3 Power Doppler has a high

 

accuracy in the detection of disease acitivity.4

 

7

Small/Large Intestine

Ulcerative Colitis

Ulcerative colitis is a continuous chronic inflammation of the distal left or even the entire colon. It manifests as an extended homogeneous slight thickening of the colonic wall with clearly identifiable wall layers and a tight lumen. There is no peristaltic activity or clear-cut hypervascularity or concurrent reaction of the adjacent tissue. On physical examination, extended diffuse tenderness may be triggered along the pathological gut signature (Fig. 7.61).

It seems possible to discriminate severe and moderate extent and activity with a specificity, sensitivity, and diagnostic accuracy of 96%, 90.3%, and 92.9% respectively.5

Fig. 7.61 Ulcerative colitis.

b Florid ulcerative colitis of the descending colon (CEUS).

a Florid ulcerative colitis of the descending colon (CDS).

 

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7

Gastrointestinal Tract

Amyloidosis

Amyloid deposits in the wall of the bowel are a rare finding: they are seen as hyperechoic, homogeneous thickening of the entire intestinal wall with filiform stenosis of the lumen (Fig. 7.62), and there is no peristalsis.

Fig. 7.62 Amyloidosis.

b Amyloidosis. Filiform narrowing of the lumen.

a Hyperechoic homogeneous thickening of the entire

 

intestinal wall.

 

Pseudomembranous Enterocolitis

Antibiotic-associated colitis/pseudomembra-

Fig. 7.63 Pseudomembranous colitis.

 

nous colitis often affects the entire colon with

 

emphasis on the distal part. This diagnosis can

 

be suspected without the proof of clostridium

 

toxin if the history allows it and if there is a

 

marked hypoechoic hypervascular swelling of

 

the intestinal wall, which can often be found in

 

this type of colitis (Fig. 7.63).

 

Ischemia

In acute ischemia there will be edematous swelling of the bowel wall and, while the layering of the wall initially persists, eventually it will end in hypoechoic thickening and narrowing of the lumen. The lack of vascularization in color Doppler ultrasound (especially since the diseases to be considered in the differential diagnosis tend to be hypervascular) raises the suspicion of a circulation disorder. Color Doppler ultrasound is not sensitive enough to detect ischemia directly. With CEUS the lack of vascularization can be seen reliably (despite earlier findings) and the extent of the ischemia may even be delineated. Further studies with CEUS in ischemia are needed (Fig. 7.64, Fig. 7.65).

Fig. 7.65 Scan shows gas in the bowel loop wall in severe enterocolitis.

Fig. 7.64 Superinfected ischemic colitis: hypoechoic swelling; almost no evidence of vascularity.

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