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Gastroparesis is delayed gastric emptying of either solids or liquids, which occurs in the absence of mechanical obstruction. Although associated with many diseases, the most frequent cause of gastroparesis is diabetes mellitus. It is estimated that up to 50% of diabetic patients may have this problem. Symptoms of gastroparesis include postprandial nausea, epigastric pain/burning, bloating, early satiety, excessive eructation, anorexia and vomiting. The vomiting associated with gastroparesis often has the following two features: (1) emesis of undigested foods ingested more than four hours previous; and (2) emesis of undigested foods in the middle of the night or in the morning prior to eating breakfast. It is important to recognize and treat gastroparesis not only to decrease symptoms but also to prevent bezoar formation and nutritional deficiencies as well as to improve glycemic control in brittle diabetics. The purpose of this article is to review the physiology of gastric emptying and to use this information to understand the pharmacological therapies for this debilitating problem.
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PMID:Gastroparesis: current management. 878 40

A 24-year-old previously healthy man presented with a 3-week history of progressively intensifying symptoms of diabetes mellitus. He had become increasingly unwell during the night preceding his admission to hospital and had developed central pleuritic chest pains with nausea; he had vomited once. On admission, he was clinically dehydrated and acidotic with Kussmaul's respiration. A diagnosis of diabetic ketoacidosis was confirmed by laboratory tests (arterial pH 7.21; bicarbonate 11.6 mmol l-1; blood glucose 40.5 mmol l-1, and heavy ketonuria). Subcutaneous emphysema was palpable in the neck tissues and a chest X-ray revealed mediastinal emphysema. There was no clinical or radiological evidence of acute or chronic pulmonary disease and a barium swallow confirmed the integrity of the oesophagus. He made an uneventful recovery from the ketoacidosis with conventional therapy. The subcutaneous emphysema and pneumomediastinum had completely resolved at review 4 weeks later.
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PMID:Pneumomediastinum complicating diabetic ketoacidosis. 879 65

Gastrointestinal symptoms are often encountered in patients with diabetes mellitus. Symptoms may arise in any region of the alimentary tract; common symptoms are heartburn, nausea, vomiting, diarrhea, constipation, fecal incontinence, and abdominal pain. This article reviews practical approaches to the identification of the pathophysiologic mechanisms involved in diabetic enteropathies and their complications and briefly outlines strategies to treat these symptoms. Particular emphasis is placed on applied physiologic tests and the choice of pharmacotherapy (e.g., cisapride, erythromycin, or octeotide). The current role of pancreatic transplantations also is briefly reviewed.
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PMID:Gastrointestinal problems in diabetes. 879 4

Alpha-glucosidase inhibitor can suppress postprandial hyperglycemia by delaying the absorption of carbohydrates in the intestine, and may be useful in obese patients with non-insulin-dependent diabetes mellitus (NIDDM) and preserved insulin secretion. We encountered an obese elderly patient with NIDDM in whom gait disturbance had developed after cerebral hemorrhage and who suffered from ileus after treatment with voglibose. The patient had received voglibose which is reported to cause fewer abdominal symptoms than acarbose, for 15 days. The patient, a 63-year-old woman, was given a diagnosis of NIDDM in February 1995, and was treated with a sulfonylurea agent. However, her glycemic control remained poor and she was admitted to our hospital in April 1995. Her body mass index was 30.5 kg/m2 and laboratory investigation revealed a fasting plasma glucose level of 211 mg/dl, a postprandial (2 h) plasma glucose level of 288 mg/dl, HbAlc of 9.9%, a fasting insulin level of 9 microU/ml, urinary C-peptide excretion of 95.7 micrograms/ day, and an coefficient of variation of R-R value of 2.1%. Fifteen days after glibenclamide was replaced by to voglibose, abdominal pain, nausea, constipation, and ausculatory sounds of gurgling developed, and niveau were noted on an abdominal roentgenogram which indicated that simple ileus had developed. Voglibose was discontinued and the patient was treated with an enema and hot air. She recovered from simple ileus on the next day. This patient had had two abdominal surgeries and a cerebral hemorrhage, and her daily physical activities were limited, which might have contributed to ileus. In elderly patients with NIDDM, a history of abdominal surgery and the amount of daily exercise must be considered when deciding whether or not to give alpha-glucosidase inhibitors.
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PMID:[Occurrence of ileus after voglibose treatment in an elderly diabetic patient with gait disturbance caused by cerebral hemorrhage]. 892

A case of Iotrolan encephalopathy is reported. A 66-year-old woman, suffering from subarachnoid hemorrhage, was admitted to our department on January 17th, 1995. After an operation for aneurysmal clipping and ventriculo-peritoneal shunt, she was discharged with no neurological deficiency. CT scan revealed ventricular enlargement and slight periventricular lucency. She was re-admitted on January 4th, 1996. She was suffering from nausea, vomiting, right hemiparesis, right hemi-hypesthesia and disturbance of consciousness. CT scan demonstrated right thalamic bleeding and bilateral ventricular hemorrhage. Further ventricular enlargement was also revealed. With medical treatment, her symptoms were relieved gradually. But disorientation and memory disturbance continued. Shuntography with Iotrolan was performed on February 2nd, 1996. The ventriculo-peritoneal shunt was demonstrated to be occluded on the abdominal side. The volume of Iotrolan used was about 8cc. She became very restless on the night of the examination. Her temperature was up to 38. CT on February 4th demonstrated brain penetration of the Iotrolan. Revision of ventriculo-peritoneal shunt, administration of steroids and hydration was performed. CSF findings demonstrated no abnormalities. Her symptoms were relieved gradually. Iotrolan is a non-ionic contrast media of dimer type, composed of C37 H48 I6 N6 O18. Its distinctive features are low distributing coefficient and high affinity with water. Contrasting several reports of Metrizamide encephalopathy, only 2 cases of Iotrolan encephalopathy were reported. Iotrolan is reported to be much safer than Metrizamide. We were able to find brain penetration by Iotrolan. It is expected to be a characteristic radiological finding of encephalopathy induced by contrast media. The mechanism of Iotrolan encephalopathy is obscure. Several theories concerning Metrizamide encephalopathy are proposed. These are (1) inhibition of hexokinase, (2) inhibition of acethylcholinesterase, (3) immunological mechanism and (4) vascular disturbance. Iotrolan has no 2-deoxy-glucose structure. The inhibition theory of hexokinase is least expected. Related matters are circulatory disturbance of liquor, dehydration, excessive contrast media, advanced age, diabetes mellitus, hypertension, epileptic patients and patients taking phenothiazines. Prompt therapy is important. Removal of contrast media, hydration and administration of steroids should be performed as early as possible.
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PMID:[A case of Iotrolan encephalopathy]. 893 76

Hyperglycemia slows gastric emptying in normal individuals and patients with diabetes mellitus and may affect both somatic and visceral sensation. The effects of hyperglycemia on proximal gastric motility and sensation during intraduodenal infusion of a triglyceride emulsion were evaluated using a barostat in six normal subjects during euglycemia and hyperglycemia (approximately 15 mmol/l). Isobaric distension induced greater bag volumes during hyperglycemia compared with euglycemia at 3 (452 +/- 26 vs. 343 +/- 12 ml, P < 0.05) and 4 mmHg (600 +/- 55 vs. 497 +/- 50 ml, P < 0.05) above basal pressure. During isovolumetric distension, intrabag pressure was less during hyperglycemia at 500 (2.5 +/- 0.3 vs. 3.5 +/- 0.5 mmHg above basal pressure, P < 0.05) and 600 ml (3.0 +/- 0.4 vs. 4.5 +/- 0.5 mmHg above basal pressure, P < 0.05). Perception of nausea (P < 0.05) and fullness (P < 0.05) was increased during hyperglycemia compared with euglycemia. We conclude that hyperglycemia 1) reduces proximal gastric tone during intraduodenal triglyceride infusion, an effect that may contribute to delayed gastric emptying, and 2) increases the intensity of nausea and fullness during intraduodenal triglyceride infusion and proximal gastric distension, indicative of an effect on visceral sensation.
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PMID:Hyperglycemia affects proximal gastric motor and sensory function during small intestinal triglyceride infusion. 894 95

The purpose of the present study was to examine the presentation and outcomes associated with diabetic ketoacidosis (DKA) in pregnancies complicated by diabetes. Eleven episodes (2%) of DKA were diagnosed during the 10-year study period. All patients were under close observation by the Diabetes-in-Pregnancy Service. Plasma glucose levels of less than 200 mg/dL were present in 4 of the 11 patients (36%), 10 (90%) of whom presented with nausea, vomiting, and decreased caloric intake. Two subsequently had fetal distress necessitating cesarean section. One fetal death occurred in a patient treated with subcutaneous insulin. Despite contemporary methods of diabetes care, near-normal plasma glucose levels are not enough to preclude diabetic ketoacidosis. Nausea, vomiting, and decreased caloric intake in an otherwise normal pregnant, diabetic woman requires evaluation to exclude ketosis.
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PMID:The changing presentations of diabetic ketoacidosis during pregnancy. 896 Jun 16

In adults with diabetes mellitus, hepatomegaly and abnormalities of liver enzymes occur as a consequence of hepatocellular glycogen accumulation, as has been well described in children. During periods of hyperglycemia glucose freely enters the hepatocytes driving glycogen synthesis, which is augmented further by administration of insulin to supraphysiologic levels. The accumulation of excessive amounts of glycogen in the hepatocytes is a function of intermittent episodes of hyperglycemia and hypoglycemia and the use of excessive insulin. Hepatic glycogenosis occurs in patients with poorly controlled insulin-dependent type I or type II diabetes. The clinical manifestations of this phenomenon may include abdominal pain and obstructive symptoms such as early satiety, nausea, and vomiting. Ascites has rarely been reported. The typical biochemical findings are mildly to moderately elevated aminotransferases, with or without mild elevations of alkaline phosphatase. Liver synthetic function is usually normal. All these abnormalities, including the hepatomegaly, are readily reversible with sustained euglycemic control. The other major cause of hepatomegaly in patients with diabetes is steatosis. This is a function of the body habitus and state of insulin resistance rather than glycemic control. However, the distinction between steatosis and glycogenosis is important: whereas steatosis may progress to fibrosis and cirrhosis, glycogenosis does not, but reflects the need for better diabetic control. Glycogenosis and steatosis cannot be distinguished reliably on ultrasound examination. The histology, however, is definitive. In glycogenosis, as in primary glycogen storage diseases, there is excess glycogen in the cytoplasm, and often also in the nucleus, of hepatocytes. The hepatocytes throughout the lobule appear pale and swollen with clearly defined cell boundaries. Ultrastructural examination reveals cytoplasmic glycogen in clumps displacing organelles to the periphery of the cell, and there is little if any steatosis. We have shown that hepatomegaly due to glycogenosis in adults with diabetes is similar in all respects to the condition seen in children. As in children, liver enzyme abnormalities are unreliable in predicting the presence or the extent of glycogenosis. Hepatic glycogenosis can occur at any age, and therefore should be included in the differential diagnosis of hepatomegaly in all insulin-requiring diabetics.
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PMID:Hepatomegaly and abnormal liver tests due to glycogenosis in adults with diabetes. 898 49

A 41-year-old black woman with a history of well-controlled, insulin-dependent diabetes mellitus was in her usual state of relatively good health when she had acute onset of right upper quadrant and epigastric abdominal pain, nausea, and vomiting. Physical examination and laboratory evaluation revealed gastrointestinal hemorrhage, decreased mental status, and acidemia, and emergency exploratory laparotomy elucidated ischemic bowel, of which 90 cm was resected. Postoperatively, the patient had cardiac arrest and could not be resuscitated. Autopsy was remarkable for mesenteric venous thrombosis and pylethrombosis, with ischemic necrosis of bowel and passive hyperemia. The arterial side of the cardiovascular system was relatively unaffected. Although arterial vascular complications of diabetes mellitus are well known, venous complications are less well described.
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PMID:An unusual complication of diabetes mellitus: the zebra that became a horse. 900 34

Hyperglycemia slows gastric emptying and increases the intensity of perception of gastric distension during fasting and small intestinal nutrient stimulation. In order to examine the possibility that abnormalities of gastric electrical rhythm may be associated with the effects of hyperglycemia, the gastric electrical rhythm (cutaneous electrogastrogram) and the perception rating scores for upper gastrointestinal sensations (visual analog scale) were examined. Studies were performed during intraduodenal triglyceride infusion in 10 healthy volunteers under euglycemic and hyperglycemic (approximately 15 mmol/liter) conditions. During fasting, hyperglycemia had no effect on either gastric electrical rhythm or sensation. Intraduodenal triglyceride infusion was associated with an increase in bradygastria (<2.4 cpm) during both euglycemia (33 +/- 9%) and hyperglycemia (36 +/- 10%, P < 0.05 vs baseline for each). During intraduodenal triglyceride infusion, tachygastria (>3.6 cpm) was more prevalent during hyperglycemia when compared to euglycemia (25 +/- 10% vs 1 +/- 1%, P < 0.05) and the perception rating scores for nausea and abdominal discomfort were greater during hyperglycemia (P < 0.05 for both). The intensity of nausea correlated with the proportion of time spent in tachygastria (r = 0.64, P < 0.01). These data are consistent with the concept that postprandial upper gastrointestinal symptoms in patients with diabetes mellitus may be modulated by the blood glucose concentration.
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PMID:Hyperglycemia affects gastric electrical rhythm and nausea during intraduodenal triglyceride infusion. 907 40


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