■ Small/Large Intestine

Small intestine. Ultrasonographic assessment of the jejunum and ileum is successful only if certain conditions are met. When differentiating sonographic findings of the small intestine, it is vital to know the time of the last ingestion. In a fasting patient these segments of the small intestine do not display a filled lumen, and unless there are pathological findings, such as ascites or inflammatory or neoplastic changes, this “empty intestine” is masked from the routine diagnostic ultrasonography. The only section of the small bowel regularly identified during ultrasound scanning is the terminal ileum where it crosses anterior to the psoas

muscle and where it terminates at the colon (ileocecal valve). Visualization and assessment of the jejunal and ileal loops can be facilitated and improved by examining the patient postprandially or after oral intake of fluid (with antifoaming agent added). Apart from a systematic analysis based on the above criteria, assessment profits from use of a 5 MHz probe since this allows better differentiation of the wall layers. In the visualization and assessment of peristaltic activity, no other abdominal organ, except the small bowel, has to rely so heavily on real-time scanning.

Colon. The large bowel frames the abdominal cavity. It is always filled to a varying degree by feces, scybala, and gas, thus being more of a hindrance for abdominal ultrasound scanning than offering easy access for diagnostic sonography. The physiological peristaltic movement of the colon cannot be visualized. The wall, lumen, and peristalsis can only be identified in large-bowel pathology or when employing special examination techniques (retrograde saline lavage, hydrocolonic sonography).

Carcinoma

Focal adenocarcinoma is a common pathological finding in the large bowel, but it is a rare entity in the small intestine (Figs. 7.24, 7.25, 7.26, 7.27). Ultrasonography will demonstrate a typical concentric or atypical off-center target sign with loss of the normal wall layers. Irregular delineation at the luminal surface is not uncommon, and in concentric malignancies quite often the lumen will be narrowed. This stenosis may result in dilatation of the intestinal segments upstream, finally leading to fullblown ileus. The area around the neoplasm is

Fig. 7.25 Cancer of the colon in a polypoid tumor with pathologic tumor vessels.

characterized by a lack of peristaltic movement. The texture of the target sign is coarse, lacks pliability, and sometimes may be painful, signifying peritonitis.

The tumor may present a smooth or irregular surface, and in advanced stages free fluid and localized lymphadenopathy around the tumor may be demonstrated. Presently, there are no clear-cut color flow Doppler criteria characteristics of intestinal malignancy. These lesions are rather hypovascular in CEUS examinations, but relevant studies are lacking.

Fig. 7.26 Cancer of the colon with target sign, dorsally ascites by peritoneal carcinosis.

Fig. 7.24 Cancer of the small intestine.

Fig. 7.27 Tumor of the cecum: in CEUS, solid tumor formation, cystic/necrotic liquefaction.

In intussusception one part of the intestine prolapses along the longitudinal axis into an immediately adjoining part. Intussusception of early childhood, where the abnormal mobility of various intestinal segments will lead to the well-known enteric (Fig. 7.34) and ileocecal intussusception, has a different etiology from that in adults. In the latter case, there will always be a lead point triggering and leading the way for the prolapse. Such lead points include polyps (Figs. 7.35, 7.36, 7.37, 7.38), large mural lymph nodes, and tumors; in addition, intussusception may also arise in small bowel affected by Crohn disease.

Intussusception will present intermittently as a multilayered pathological gut signature or target sign. Edema and inflammation produce marked thickening, thus emphasizing the various layers of the wall, the outermost hypoechoic layer (muscularis propria) of the intus-

Fig. 7.34 Enteric intussusception.

Besides the typical clinical findings, ultrasound has become the most important method for the diagnosis of diverticulitis, providing a sensitivity of 98.1% and a diagnostic accuracy of 97.7%.

Diverticula of the sigmoid colon are echogenic because of the gas or feces they contain; sometimes the outer hypoechoic layer of the intestinal wall (muscularis propria) becomes more pronounced owing to the concurrent muscular hypertrophy.

At times, duodenal diverticula (Fig. 7.43, Fig. 7.44) may be recognized at the papilla by the manifestation of indirect signs such as dilation of DP and/or DHC and by the alternating presence of air and fluid within the lumen. A malignant mass has to be excluded (by CEUS). However, Meckel’s diverticulum may only be visualized in the presence of pathological changes.

Fig. 7.43 Visualization of a periampullary duodenal diverticulum filled with air.

Fig. 7.44 Parapapillar duodenal diverticula with dilated pancreatic and common bile duct.

Diverticulitis

Inflammation of a diverticulum will always result in localized tenderness. The diverticulum itself displays marked distension; the diverticular wall will appear as an edematous, hypoechoic, crescent-shaped halo around the lumen which, when filled with feces, will be hyperechoic or hypoechoic in the presence of fluid (Fig. 7.45).

Apart from this typical local finding, diverticulitis will demonstrate two other characteristic findings: particularly proximal of the diverticulum, the intestinal loop shows extended muscular hypertrophy of the wall and thicken-

ing of the outermost hypoechoic layer, as well as edema with pronounced layering of the wall and marked narrowing of varying degree of the gut lumen. There will be significant inflammatory hypervascularity at the diverticulum, which is surrounded by a localized massive reaction of the adjacent tissue: its being walled off by the greater omentum may result in a hyperechoic halo several centimeters thick. Complications are heralded by peridiverticular fluid, local collection of gas, abscess formation, and fistulization ( 7.2).

Fig. 7.45 Diverticulitis. Indicating sign is the extensive edematous pathological gut signature in the left lower quadrant with muscular hypertrophy of the intestinal wall and narrowed lumen.

Diverticulosis/Diverticulitis

True diverticula are sacculations of the intestinal wall involving all layers and resulting in localized outpouching, e. g., duodenal diverticula (Fig. 7.43), Meckel’s diverticulum, diverticula of the ascending colon. However, false diverticula, also known as pseudodiverticula, are by far more frequent: here, gaps (defects) in the muscularis propria lead to localized sacculation of mucosa and submucosa (e. g., sigmoid diverticula). Local findings always include hyperplasia of the muscularis propria, and the

musculature of the surrounding intestinal wall becomes hypertrophied. The formation of numerous pseudodiverticula in the sigmoid colon (diverticulosis) is seen as a sequela of local pressure increases within the intestinal lumen, which in turn arises from nutrition low in dietary fiber. In addition, focal weakening of the bowel wall around the afferent and efferent vessels is also considered a causative factor. Feces impacted and inspissated in the extruded diverticular sac induce local pressure ero-

sion of the mucosa, chronic inflammatory granulation (diverticulitis), and also possibly abscess formation and perforation ( 7.2). Apart from muscular hypertrophy of the intestinal wall (particularly of the proximal segments), recurrent and chronic inflammation with edema and narrowing of the lumen will finally result in cicatricial contraction of the chronically inflamed bowel segment.

Acute appendicitis can be diagnosed sonographically with a positive predictive value of 95.7% and a sensitivity of 88.5%. Thus, the diagnostic accuracy of ultrasound is only marginally less than that of bolus CT (sensitivity 96%, positive predictive value 95–96%). Inflammation of the appendix is characterized by enlargement, dilatation, and thickening, initially with demonstration of edema and accentuated layering of the wall; quite often fecaliths will be seen within the lumen. Appendicitis is always accompanied by localized tenderness (Figs. 7.47, 7.48, 7.49). Advanced stages will destroy the layered structure of the wall and produce a hyperechoic echo, local accumulation of fluid, and abscess formation (Table 7.4, Fig. 7.50). In such an advanced stage of the inflammation, the appendix itself is almost im-

possible to identify, and frequently localized lymphadenopathy will be evident.

Table 7.5 summarizes the differential diagnosis of appendicitis by ultrasound (Fig. 7.51).

Table 7.4 Sonographic signs in acute appendicitis

●Swelling of the appendix

●Thickening of the wall

●Fluid-filled lumen

●Tenderness

●Fecalith

●Hyperechoic omental cap

●Free fluid

●Perityphlitis

●Loss of peristalsis