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Chapter 37 (page 183)
Disturbances in gastrointestinal motility with associated symptoms such as vomiting,
diarrhoea and constipation have long been recognized as complications of diabetes
mellitus. Rundles (1945) described 4 diabetic patients with diarrhoea or alternating
diarrhoea and constipation who also had pronounced anorexia and nausea. Radiological
examination in all revealed abnormal gastric retention.
Kassander (1958) described 6 cases of poorly controlled diabetes mellitus with upper
gastrointestinal manifestations, a condition he called "gastroparesis diabeticorum". In all
cases the stomach showed sluggish peristalsis with retention of barium. There was no
evidence of an organic lesion causing obstruction and all cases had a patulous pylorus
through which the gastric contents could be expressed by hand. It was concluded that
these cases represented a disturbance of propulsion, and more specifically of expulsion,
of gastric contents. The gastric retention was considered to be similar to that occurring
after truncal vagotomy and to be due to diabetic neuropathy involving the vagus nerves.
The gastric manifestations could also occur in asymptomatic diabetic patients.
Marshak and Maklansky (l964) mentioned 4 similar cases and reiterated that diabetic
gastropathy consisted of gastric retention in the absence of an obstructing lesion at the
pylorus. In some cases there was a marked decrease in peristalsis while in others
peristalsis was normal.
Zitomer et al. (l968) found that gastric neuropathy typically occurred in patients with a
long history of inadequately controlled, moderately severe diabetes mellitus. The
symptoms were generally mild and nonspecific, vomiting of undigested food from the
previous day being one of the main manifestations. Radiologically the most constant and
striking finding, occurring in 34 of their 35 cases, was sluggish, ineffectual and
irregularly occurring peristalsis; on occasion peristalsis was absent altogether. There
appeared to be decreased or absent propulsive motor activity, associated with abnormal
gastric retention of food residues and barium, resembling a bezoar. The malfunction of
gastric emptying and consequent unpredictable food absorption probably contributed to
poor diabetic control. Despite the considerable delay in gastric emptying, barium could
invariably be expressed by palpation through the pylorus, which remained patulous. If
the patient was placed on his right side, passive gravitational emptying of liquid contents
occurred, while solids tended to be retained. Overall the incidence of clinically
significant gastric neuropathy was extremely low in diabetes mellitus, a figure of less
than one per cent being mentioned.
Goyal and Spiro (l971) agreed that clinical manifestations of diabetic gastropathy
occurred in a very small proportion of cases. While the gastric retention resulting from
the reduction of peristaltic contractions resembled the hypomotility of truncal vagotomy,
suggesting an autonomic neuropathy, other factors might play a role. It was known, for
instance, that hyperglycaemia as well as glucagon inhibited gastric motility.
Scarpello et al. (l976) measured the rate of emptying of isotopically labelled solid meals,
using 99mTc-labelled sulphur colloid as a marker and a gamma camera. The
gastric emptying rate in 29 insulin-dependent well-controlled diabetics was compared
with that in l8 normal controls. No statistically significant difference in gastric emptying
rate between controls and diabetics with or without autonomic neuropathy was found.
Only 3 diabetics had greatly delayed gastric emptying, but in one of these the test had
previously given a normal result.
Campbell et al. (l977) used a double isotope scintiscanning technique in order to
differentiate between solid and liquid emptying in 12 patients with diabetes mellitus (6
with and 6 without objective evidence of autonomic neuropathy), and in 20 non-diabetic
controls. Gastric stasis was demonstrated in 3 patients with autonomic neuropathy. In
patients without stasis the normal differentiation between solid and liquid emptying was
impaired, suggesting an abnormality of "antral" peristalsis.
Gramm et al. (l978) reviewed the radiological findings in 43 patients with diabetic gastric
neuropathy. (It was said that the condition was seen more often on account of the
increased longevity of diabetic patients). In the majority the stomach had an elongated,
sausage-shaped configuration; there was sluggish, irregular gastric peristalsis with
retention of solid food and barium in the absence of an organic obstruction at the pylorus.
Feldman et al. (l979) found that many patients with longstanding, insulin-dependent
diabetes mellitus had reduced acid secretory responses to sham feeding (suggesting vagal
neuropathy) and normal responses to infused food. Both in diabetics with nausea and
vomiting and in patients without upper gastrointestinal symptoms, abnormal gastric
retention of a nonabsorbable meal marker occurred. The findings supported earlier
observations that gastric secretory and motor functions could be impaired in
Malagelada et al. (l980) studied gastric motility by means of pressure transducers in the
fornix, "antrum" and duodenum in fasting diabetic patients with symptomatic
gastroparesis, as well as in asymptomatic diabetics and normal controls. Healthy subjects
and asymptomatic diabetes mellitus patients averaged 2 phase III migrating motor
complexes per 180 minutes, while most diabetics with gastroparesis had no such
complexes. Whether analogous "antral" muscle dysfunction occurred postprandially in
diabetic patients with gastroparesis was uncertain. However, as the emptying of solids
might be delayed, it seemed likely that "antral" motor activity could be abnormal as it
was the main mechanism responsible for the emptying of solids (Chap. 18).
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