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Diabetes and Gastroparesis

Posted on September 9, 2018 | No Comments on Diabetes and Gastroparesis

Gastroparesis is a long-standing disorder of the stomach characterized by delayed emptying of the stomach in the absence of mechanical obstruction. Simply put, the stomach takes too long to empty its contents. Gastroparesis may present with a variety of symptoms, which include early satiety, nausea, vomiting, bloating, and upper abdominal discomfort.

A recognized complication of diabetes mellitus, gastroparesis classically is considered to occur in those individuals with long standing diabetes mellitus. Many affected patients also have disorders of the autonomic nervous system which regulates movement and secretion in the gastrointestinal tract, including postural hypotension. Delayed gastric emptying is present in about 25 to 55 percent of patients with type 1 diabetes mellitus, while it has also been described in approximately 30 percent of patients with type 2 diabetes mellitus. Fortunately, not all diabetics will develop gastroparesis, and unlike traditional beliefs, its presence does not mean poor prognosis for these patients.

Clinically, important consequences of diabetic gastroparesis include the development of gastrointestinal symptoms, malabsorption of food and drugs, and destabilization of blood sugars. Symptoms in affected diabetic patients include nausea, vomiting, early satiety, fullness, and abdominal discomfort. The presence of abdominal bloating and fullness seems to be associated with the magnitude of emptying delay. Symptom severity, however, does not necessarily correlate well with the amount of delay in gastric emptying. Some patients with severe symptoms may have near-normal to normal emptying patterns. In these individuals, other abnormalities, including abnormal pain perception resulting to discomfort to even normal stimulus, may be potentially responsible for dyspeptic symptoms in these patients.

Apart from development of symptoms, changes in gastric emptying may affect blood sugar levels after meals. Delayed stomach emptying contributes to poor control of blood sugar because of unpredictable delivery of food into the small intestines where it is absorbed into the blood stream. This, together with continued administration of insulin may produce hypoglycemia (low blood sugar). On the other hand, acceleration of emptying with medications has been reported to cause hyperglycemia (high blood sugar). Problems with blood glucose control may be the first indication that a diabetic patient is developing gastroparesis.

Diabetic gastroparesis is likely to result from impairment of nerve control of gastric motility, possibly at the level of the vagus nerve. In one study, abnormalities of nerves in diabetic patients were not identified by microscopic examinations, but there was note of abnormal transmission in these nerve tracks. On the other hand, signs of inflammation in some parts of the autonomic nervous system were noted in previous studies.

Hyperglycemia alone also may affect emptying of the stomach and reduce the effectiveness of medications. Normalization of blood glucose levels has been shown to stabilize gastric electric activity and improve gastric emptying.

Glucose-responsive nerves have been identified in the central nervous system* that may modify activity of the autonomic nervous system. Substances like prostaglandins may also be involved in the inflammation, because indomethacin can reverse abnormal electrical abnormalities in the stomach that occur during hyperglycemia in healthy volunteers. Patients with type 1 diabetes mellitus also exhibit increased perception of distention of the stomach, with exaggerated nausea, fullness, and epigastric pain for a given distending stimulus. In addition, hyperglycemia increases nausea and fullness when the stomach is distended. Increased sensitivity of the stomach may be responsible for after-meal discomfort when the stomach is distended by food.

Gastroparesis is diagnosed by demonstrating delayed gastric emptying in a symptomatic individual after exclusion of other potential causes of symptoms. Typical symptoms in an individual with long-standing type 1 diabetes mellitus suggest diabetic gastroparesis. Most important in patients who are suspected to have gastroparesis is to exclude the possibility that one is dealing with mechanical obstruction, either by endoscopy or x-ray exams. Test for measurement of gastric emptying may be employed if available, but most of the time, a strong clinical suspicion in the absence of mechanical obstruction may already warrant empirical treatment with available prokinetic agents or drugs that help stimulate stomach muscles to contract.

The general principles for treatment of symptomatic gastroparesis are the following: (I) correct fluid, electrolyte, and nutritional deficiencies; (2) identify and rectify the underlying cause of gastroparesis if possible; and (3) reduce symptoms.

The patient’s medication list should be reviewed to eliminate drugs that might exacerbate the underlying motility disorder or prevent the beneficial actions of a prokinetic agent. Diabetic patients should strive for optimal glycemic control to minimize any inhibitory effects of hyperglycemia on gastric emptying.

For relatively mild disease, dietary modifications by increasing liquid content of food and a low-dose antinausea or prokinetic agent might provide satisfactory control of symptoms. Patients with more severe manifestations of gastroparesis, such as refractory vomiting, pronounced dehydration, or erratic blood glucose control would require hospitalization, intravenous hydration, nasogastric decompression of the stomach, giving insulin for blood glucose control, and intravenous administration of antiemetic agents, which decrease vomiting, and prokinetic agents which promote forward movement of the stomach and the rest of the gastrointestinal tract. As with the diagnostic approach to gastroparesis, most recommendations regarding its treatment are based on the cumulative experience and opinions of clinicians who specialize in the care of these patients.

The following prokinetic drugs can be used in the treatment of gastroparesis: metocloparamide, erythromycin, domperidone, tegaserod and bethanechol.

For refractory cases, drug combinations may be tried, albeit studies are lacking in the effectiveness of these regimens. Surgical treatment is generally not recommended, although insertion of a jejunal feeding tube may be helpful in maintaining nutritional needs of these patients.

Newer treatment options, aside from newer prokinetic agents presently being studied include the use of botulinum toxin injection to relax the pylorus and the use of “gastric pacing” stimulators similar to that of a cardiac pacemaker, to modulate gastric emptying. However, these methods are still in the investigational stage and not being recommended for clinical use at the present time.

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