Chapter 37 (page 184)

The Pyloric Sphincteric Cylinder in Health and Disease

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Chapter 37 (page 184)

According to Feldman and Schiller (l983) the pathogenesis of diabetic gastroparesis remained uncertain, but the evidence supported the view that a vagal autonomic neuropathy was responsible. Feldman et al. (l984), using a radioloic method for assessing gastric emptying of radio-opaque, indigestible solid particles with simultaneous radionuclide scintigraphy of an ¹¹¹In-labelled standard meal, showed that patients with insulin-dependent diabetes mellitus had an abnormally slow gastric emptying rate for indigestible solids; emptying of digestible solids and liquids was close to normal.

Camilleri and Malagelada (l984) studied the fasting and fed manometric profiles of the stomach and proximal small intestine in 14 patients with the clinical diagnosis of diabetic gastroparesis. In 11 of the patients reduction in "antral" pressure activity with absent interdigestive migrating motor complexes was seen. Three patients exhibited a "peculiar continuous 3 minute antral contractile activity". In the small intestine abnormal manometric patterns were observed in 12 patients, in 9 of whom non-propagated, long bursts of powerful contractions occurred. The findings indicated that both in the stomach and small bowel the motility disorder was not invariably of a paretic type. In the stomach a reduction in frequency of amplitude of "antral" motor activity was the rule, but in a minority of patients prolonged periods of contraction of low amplitude (less than 20 mm Hg), occurred. This motor pattern indicated an abolition of the physiological cyclic activity and was distinctly abnormal; the consistently low amplitude might be insufficient to triturate solid food and empty the stomach. Clinically these patients had the same symptoms as those with "antral" hypomotility, for whom the term gastroparesis was perhaps more appropriate.

In symptomatic diabetic gastroparesis patients Achem-Karam et al. (l985) demonstrated abnormal "antral" and duodenal activity, characterized by absence of phase III of the interdigestive migrating motor complex; in 3 out of 6 patients the complex was also absent in the remainder of the proximal small bowel. The findings confirmed some of those previously described by Malagelada et al. (l980) and Camilleri and Malagelada (l984).

Using a dual radionuclide technique, Wright et al. (l985) investigated gastric emptying of solids and liquids in diabetic gastroparesis patients and normal controls. In both groups the emptying rate of liquids was normal; emptying of solids was markedly delayed in the diabetic group.

With a similar technique Horowitz et al. (l987) determined the effects of the prokinetic drug cisapride in 20 insulin-dependent diabetic patients who had delayed gastric emptying of the solid or liquid component of a meal, or both. It was found that cisapride increased the emptying rate of both solids and liquids.

Yoshida et al. (l988) found no morphologic abnormalities of the abdominal vagus nerves, the gastric musculature and myenteric plexuses in patients with diabetic gastroparesis.

In a review Varis (l989) defined diabetic gastroparesis as a delay of gastric emptying without gastric outlet obstruction in patients with long-standing insulin requiring diabetes mellitus. Characteristically the emptying of solids was delayed; in most cases the emptying rate of liquids was within the normal range, although it might be decreased in some patients. All normal motility patterns, e.g. adaptive relaxation and the maintenance of tone in the proximal stomach, "antropyloric" peristaltic movements and phase III of the interdigestive migrating motor complex might be lacking or abnormal. The "antral" motility disorder, leading to retention of solid foods, was considered to be the most characteristic feature of the condition.

As endoscopy may fail to demonstrate motor disorders of the stomach (Varis l989), it does not play an important role in the diagnosis. However, endoscopy does show gastric mucosal pathology such as acute erosions and gastritis, occurring in the majority of patients with diabetic ketoacidosis (Carandang et al. l969), and it may help to exclude mechanical pyloric obstruction (Camilleri and Malagelada l984).

From the above it is clear that gastric motility disturbances may occur both in symptomatic and asymptomatic diabetes mellitus patients. In a small percentage of cases these disorders may progress to diabetic gastroparesis, a condition usually occurring in patients with a long history of inadequately controlled, insulin-dependent diabetes mellitus.

We have had occasion to do upper gastrointestinal radiological examinations in numerous diabetic patients for a variety of reasons, over a period of years. Motility disturbances were found in a small number of patients, both in insulin-dependent and non-insulin dependent cases.