Most of us have experienced difficulty at times in deciding whether a small intestine is normal or abnormal by roentgen examination, and further, if abnormal, what name to give to the condition. Different workers use different procedures, administer the barium in different mixtures, and use different terms to describe the resulting radiographic appearances. There is a widespread desire for reliable criteria for the limits of normal and for the best possible examination procedure. We find that suspensions in water of barium sulfate and the sodium salt of methylcarboxycellulose4 are stable and inert physiologically, have a rapid small-intestine transit time, and produce a good mucosal pattern in patients without small-intestine disease. Zimmer (1) made extensive studies of the settling of barium (in vitro and in vivo) in distilled water, in hard tap water, in artificial gastric juice, and in artificial intestinal juice. He found that pure barium produces a coarsened mucous membrane pattern and segmentation. He says that when “protective colloids” are added a “gracefully barbed” mucosa shows up. The preparation he recommends activates peristalsis so that the entire small intestine can be visualized in an hour. Frazer, French, and Thompson (2) showed how the “segmentation pattern” could be induced in normal subjects. They gave, at different times, a long list of substances with barium by mouth and by duodenal tube. The following produced segmentation: hypertonic saline, sodium bicarbonate, and glucose; also sodium oleate, hydrolyzed olive oil, sprue fecal fat, and olive oil. They also found that an abnormal small bowel pattern was induced in a healthy individual by the ingestion of a fatty meal the evening before the examination. Experiments in vitro showed that when mucus was added, fluocculation resulted. There was the same picture when barium mixed with mucus was placed in a loop of intestine removed from a cadaver. Frazer and his associates believed that the segmentation pattern they induced in normal people was indistinguishable from the “deficiency pattern.” It would seem that altered neuromuscular activity, as suggested by Golden, is not the correct explanation for this phenomenon for it could not account for the changes observed in the normal small bowel examined postmortem. That the segmentation pattern is associated most often with defective fat absorption was shown not only by these authors, but also by Snell and Camp (3), Gambill (4), and Kantor (5). The conditions which may produce it are: tropical and non-tropical sprue, celiac disease, obstructive jaundice, pancreatic fibrosis of infants, pancreatogenous diarrhea (Kirklin), mesenteric lymphatic obstruction, and Whipple's disease. Gambill, in a study of patients with pancreatic calcification, found steatorrhea in 32 per cent of those giving a history of pancreatitis.
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