Although often believed to be more common in patients with type 1 diabetes, it is actually also quite common in patients with type 2 diabetes. In one study of diabetic patients receiving oral hypoglycemic therapy, 30% were found to have delayed emptying of solids.⁶

A substantial proportion of patients with either type 1 or type 2 diabetes mellitus have scintigraphic evidence of delayed gastric emptying of radiolabeled solid meals, which may or may not manifest in clinical symptoms.^2,6,7 Conversely, many patents may have symptoms such as nausea, vomiting, early satiety, bloating, and abdominal discomfort or pain and yet have normal gastric emptying.

Diabetic gastropathy is thought to be a manifestation of autonomic neuropathy. The underlying cause of diabetic neuropathy, as well as other complications of diabetes, is hyperglycemia.⁸ While the entire gastrointestinal tract may be affected by autonomic neuropathy, we have a growing awareness of the role of the diabetic stomach in particular as the locus of a vicious cycle of delayed gastric emptying, poor glycemic regulation, and ascending hyperglycemia.^6,9,10

The purpose of this brief review is to focus attention on the importance of early intervention in the development of diabetic gastropathy in order to prevent the debilitating symptoms associated with it and to improve quality of life.

The second pathway is enhanced activity of the polyol pathway, in which glucose is converted to sorbitol via the enzyme aldose reductase. This results in a decrease in tissue myoinositol, with far-reaching effects throughout the nervous system. As the integrity of cellular information, including the sodium-potassium ATPase system, is disrupted, nerve conduction velocity is diminished and the anatomy of nerve fibers is altered.¹¹

Diabetic neuropathy can impair function anywhere in the nervous system. In the gastrointestinal tract, it causes, in effect, an autovagotomy.¹² In addition, hyperglycemia results in cellular anatomic disruption throughout the gastrointestinal tract, but especially in the stomach. Nerve cells may swell with the loss of myelinated fibers, and smooth muscle cells may become rounded and hyalinized. In the stomach, motility may be reduced in the antrum and proximal stomach. There may also be pylorospasm.

Hyperglycemia also has secretory effects in the stomach, including decreased secretion of hydrochloric acid.¹³ The net result of these changes is a reduction in effective emptying, starting first with indigestible solids, then progressing to digestible solids, and eventually to liquids.¹⁴ The myoelectric and neuroanatomic consequences of hyperglycemia may be accentuated by abnormal secretion of various hormones, including glucagon, gastrin, cholecystokinin, and gastric inhibitory peptide in patients with diabetes.³

Gastropathy can contribute to bezoar formation and intestinal obstruction, ulcer development, acute gastric dilatation during ketoacidosis or after endoscopy, incapacitating vomiting, respiratory aspiration, and dehydration.³ In addition to impairing quality of life and compromising nutrition, gastropathy can wreak havoc on attempts to control blood glucose through insulin administration timed to meals.

Gastropathy may further retard the entry of oral medications, including hypoglycemics and pancreatic enzymes, into the bloodstream.¹⁵ Erratic absorption of nutrients and medications may result in misleading blood glucose readings, and significant hyperglycemia may occur if blood glucose levels rise out of proportion with the expected effects of insulin.³ On the other hand, slow absorption of food may lead to hypoglycemia. The toxic effect of hyperglycemia may acutely aggravate the gastropathy,^9,16,17 possibly by reducing activity of both nerve and muscle.

Gastropathy may be underrecognized in clinical practice because the symptoms, if present, are nonspecific. Furthermore, the degree of gastropathy correlates poorly with the severity of gastrointestinal symptoms or with other evidence of peripheral neuropathy.^3,5 The reverse is also true: dyspeptic symptoms do not confer a diagnosis of gastropathy in every diabetic patient.

Unusual answers or unresponsive behavior should be followed up as diligently as positive responses. Positive responses might be, "I've been feeling a little nauseous after I eat" or, "I think I've had the stomach flu for a few weeks" or, "I seem to be losing weight without trying."

Initially, however, symptoms may not be evident, or symptoms compatible with gastropathy may in fact indicate a different disorder, such as chronic cholecystitis or gastro-esophageal reflux. Early treatment of asymptomatic gastropathy may forestall further progression of this neuropathic condition and its direct and indirect consequences.

If a patient with diabetes has lost control of his or her glucose management for no apparent reason and has no gastrointestinal symptoms, it is nevertheless important to evaluate the possible causes for a digestive or absorption problem that could be upsetting the glycemic balance. This includes investigating the possibility of delayed gastric emptying due to a variety of causes (Table 2). A differential diagnosis algorithm should be followed to determine whether the patient has early or asymptomatic diabetic gastropathy that is interfering with a previously effective treatment regimen.

Although diabetic gastropathy is most common in patients with long-standing insulin-dependent diabetes, it also occurs in patients who do not require insulin and in those in whom diabetes has been only recently diagnosed. It should be noted, however, that many patients with type 2 diabetes may have had the condition for many years before diagnosis.

Diabetic gastropathy is frequently associated with other diabetic complications, such as retinopathy, peripheral neuropathy, and nephropathy. Thus, it can be helpful to determine the degree of neuropathy in other systems.

Other components of the medical history include a careful drug history to rule out use of narcotics, tricyclic antidepressants, anticholinergics, and other agents that can slow gastric motility as listed in Table 2.

If the cause of gastropathy is not clear, or if either the laboratory or physical examination results are suspicious, the next step in diagnosis is an upper gastrointestinal series or endoscopy to rule out mechanical obstruction of the duodenum, small bowel, or stomach. If the findings of these procedures are positive, the next step is to treat the cause of the obstruction. However, if bezoars—solid balls formed in the digestive tract—are found, gastropathy should not be ruled out. These obstructions may be the result of delayed gastric emptying. Bezoars may contain vegetable matter, sometimes mixed with hair, or incompletely digested or undigested food that has not been passed on through the alimentary system.

Patients with diabetes may have gastropathy concomitant with another condition that causes suspicious signs and symptoms. Among these are obstruction by an ulcer or neoplastic overgrowth. Also, mechanical obstruction can be caused by pyloric stenosis, prepyloric ulcer, scarring from prior ulcers, chronic ulcer disease, or neoplasia. Other conditions that might produce a similar symptom complex include nonulcer dyspepsia, irritable bowel syndrome, and gastritis from Helicobacter pylori.

If x-ray and endoscopy reveal no obstruction, the next step is a gastric emptying scan. The test is usually interpreted as percent of emptying at a specific time after ingestion or in the time to 50% emptying. However, delayed emptying is not the definitive diagnosis of gastropathy, but only of gastroparesis, the final stage of the process. A patient may have symptoms of gastroparesis indicating a motility disorder without delayed emptying.

Therapy may include use of agents to promote gastric emptying, facilitating glucose regulation. Controlling diabetes is important to protect autonomic nerves from ongoing damage caused by high blood glucose levels. However, when severe autonomic nerve disease is present, tight blood glucose control may be counterproductive. When long-term diabetes is present, patients may not be able to detect the usual signs of hypoglycemia, such as tingling around the mouth or tachycardia. In such circumstances, it may be preferable to be more lax in controlling blood glucose since the development of unrecognized hypoglycemia can be fatal.

Clinicians can help patients accept new eating patterns, such as liberalizing the amount of starch, sugar, and easily digested carbohydrates. Patients can learn flexible insulin regimens that allow them to adjust insulin to the meal and cover carbohydrates, which are more easily digested than foods that delay gastric emptying, such as high-fiber foods, fats, and high-protein foods.

Smoking is known to delay gastric emptying. It is essential for a wide variety of health reasons to urge patients who smoke to stop. Have on hand information about local smoking cessation programs.

Exercise can be beneficial for patients with diabetic gastropathy. In addition to conferring the well-known benefits of helping to control weight and improve circulation, it may actually reduce the risk of delayed emptying by normalizing blood glucose. Patients should be advised to avoid exercise during periods of poor metabolic control, however, because blood glucose may actually rise rather than fall.

Patients and the therapeutic team should identify a blood glucose range that is as near to normal as possible while avoiding excessive hypoglycemia, such as a premeal blood glucose level of 100­140 mg/dl. The relation between elevated blood glucose levels and gastropathy symptoms should be pointed out and emphasized.

Help patients to identify postprandial blood glucose levels that mark appropriate and inappropriate glucose concentration. Use these data to understand meal digestion and the time of medication for meal coverage. Plan frequent blood glucose monitoring before and after eating. Determine a goal range for HbA_1c levels.