Pyloric stenosis causing a gastric outflow obstruction in most instances causes gastric dilatation, as described above. Vigorous
contractions may be observed without propagation of gastric contents through the pylorus and into the duodenum, although as
mentioned, gastric atony can occur over time as the stomach tires. Chronic hypertrophic pyloric gastropathy has been described
as concentric hypoechoic thickening of the pylorus. Congenital pyloric stenosis may look similar. In one case of congenital
pyloric stenosis the wall was thickened and relatively hyperechoic with poor visualization of wall layers. Focal mass lesions
of the pyloric outflow tract or irregular wall thickening may represent neoplasia or inflammatory lesions. Mass lesions, either
malignant or benign (e.g., benign polyps) may be seen projecting into the pyloric lumen. The ultrasound findings discussed
above may be confirmed with a barium or iodinated contrast material upper gastrointestinal examination. In many instances,
the diagnosis is clearly evident when information from both imaging modalities is considered. Endoscopy is an effective diagnostic
tool to further evaluate the gastric outflow tract.
Diffuse thickening of the stomach is often indicative of nonmalignant disease such as parvovirus infection, lymphocytic/plasmacytic
or eosinophilic infiltrate, uremic induced gastritis or gastritis for other causes such as dietary indiscretion. Lymphosarcoma
and mast cell disease are neoplastic diseases to consider when the stomach wall is diffusely thickened. Minimal thickening
usually preserves the normal layered appearance of the stomach wall on an ultrasound examination. Severe thickening usually
obliterates these layers. Rugal folds also become thickened. Mineralization of the gastric mucosa that may occur with chronic
renal disease has been described sonographically as a hyperechoic line at the mucosal-luminal interface, usually without acoustic
shadowing. Lymphosarcoma is the most common diffuse neoplastic disease of the stomach. The gastric wall becomes uniformly
hypoechoic and thickened with loss of normal layers. Gastric lymphosarcoma can also be a focal disease. Regional lymphadenopathy
can be indicative of the severity of gastric disease; more severe lymphadenopathy is usually associated with neoplasia. Differentiation
between these various diseases requires integration of the signalment, clinical signs, lab data, radiology interpretation,
etc. Ultimately, a fine needle aspirate or biopsy may be necessary to make a final diagnosis.
In most instances, focal gastric lesions represent a neoplastic process. Mass lesions of the stomach are identified as focal
areas of gastric wall thickening. These lesions usually obliterate the normal layered ultrasonic anatomy of the stomach wall
and can become quite large. Their appearance may be homogeneous or very complex. Gastric dilation is often present. Gastric
carcinomas, lymphosarcoma, leiomyoma and leiomyosarcoma are examples of focal gastric neoplasia. Lesions can be readily biopsied
with ultrasonic guidance. As mentioned previously, misdiagnosis of a gastric mass lesion or diffuse thickening can occur when
the stomach is assessed when empty.
Gastric ulcers are difficult to detect reliably with an UGI, but a double contrast gastrogram may be more rewarding. Evaluation
of the wall of the stomach for extensions of barium and adjacent wall thickening are the classic signs. Plication of rugal
folds, converging to a focal accumulation of barium is diagnostic (spoke wheel sign). Ultrasound has been used to diagnose
gastric ulcers. A hyperechoic area representing gas accumulation within a focal area of gastric wall is seen. There is usually
a noticeable depression in the mucosal surface. Gastric fluid distension is often present and regional reduction in gastric
wall peristalsis may be observed. The area surrounding the gastric ulcer should be studied for evidence of focal perigastric
fluid accumulation and hyperechoic mesentery, evidence of ulcer perforation and focal peritonitis. Ultrasound may be used
to assess gastric ulcer healing, with reduction of wall thickness and eventual reestablishment of normal wall layering. Care
must be taken to differentiate trapped air bubbles within gastric rugae from true gastric ulcers.
Much can be learned about the small intestine (SI) from survey abdominal radiographs if a few basic guidelines are kept in
mind. First, intestinal contents should be assessed. The typical canine small intestine contains a mixture of both fluid
and gas. A totally fluid-filled or gas-filled SI in dogs is usually a sign of disease. The cat SI contains predominately
fluid. Granular, calcific material is not normally present in the SI of either the dog or cat. Its presence is highly suggestive
of some form of obstructive process, usually a long-standing partial obstruction.
Bowel diameter is another criteria to be assessed on survey abdominal radiographs. A good rule-of-thumb is that SI diameter
should not exceed the height of the body of the lumbar vertebrae in dogs, or around 12 mm in cats. Bowel diameter exceeding
these criteria suggests some form of pathology. If the SI is diffusely enlarged, this is a fairly easy task. More of a challenge
is detection of focal SI dilatation on the survey radiographs. The diameter of the intestinal loops can be reliably evaluated
during the UGI. Dilated loops of bowel indicate ileus, either functional or mechanical. "Stacked" loops of gas distended
bowel often indicate an obstructive process.
An attempt should be made to locate and visualize the cecum and entire colon (ascending, transverse and descending). It is
important to differentiate small intestine from large intestine because colonic diameter will usually exceed that of the small
bowel, and the contents of the colon will be granular and sometimes calcific. This is normal for the colon, abnormal for the
The barium column should be continuous as it leaves the stomach and enters the small intestine. Fragmentation of the barium
column within the SI may indicate delayed or intermittent gastric outflow, abnormal peristalsis, or altered SI physiology
(e.g., altered pH, excessive mucus, etc.). Barium often reaches the colon in the dog in 2 hours, as soon as 30 minutes in
the cat. Barium should be cleared from the small intestine of the dog by 5 hours, 3 hours in the cat.
The intestinal walls should be evaluated for thickness. Wall thickness in the dog and cat is typically 2-4 mm in the jejunum
and ileum, slightly thicker in the duodenum. The mucosal surface is assessed for irregularity or filling defects. The gastrointestinal
tract as seen sonographically as alternating hyperechoic and hypoechoic layers, whether viewed in long-axis or in cross-section.
Optimally, five discrete layers of the GI tract can be seen, corresponding to the luminal/ mucosal interface, mucosa, submucosa,
muscular layer, and the serosa.
The constant movement of the intestinal tract due to segmental and peristaltic contractions can produce some unusual appearances
of the contrast medium column. To avoid mistaking a contraction or peristaltic wave for a pathologic lesion, the area of
suspicion should be seen on additional radiographs (i.e., the more times you see it, the more likely it is to be a true lesion).
Peristaltic activity varies when small bowel dilation is present, from complete absence to hypermotility. Hypermotility is
probably more common with acute mechanical obstructions from foreign material and infectious or dietary induced enteritis
than with chronic partial obstructions. Two distinctive normal patterns of the proximal SI need to be recognized radiographically.
One is the "string of pearls" appearance of the cat intestine, which is simply peristalsis. The pattern is often mistaken
for a linear foreign body. The second pattern is the "pseudoulcer", smooth depressions along the antimesenteric border of
the canine duodenum that represent filling defects from islands of lymph tissue.