Diabetic Gastroparesis

Gastroparesis is a complication of long-standing type 1 and type 2 diabetes mellitus. Symptoms associated with gastroparesis include early satiety, prolonged postprandial fullness, bloating, nausea and vomiting, and abdominal pain. Mortality is increased in patients with diabetic gastroparesis. A subset of patients with diabetic gastroparesis have pylorospasm that results in obstructive gastroparesis. Current treatment approaches include improving glucose control with insulin and prescribing antinauseant drugs, prokinetic agents, and gastric electric stimulation. Future directions include improved diet counseling based on gastric emptying rate, continuous insulin delivery systems with glucose sensor-augmented monitoring, and drugs for correcting gastric neural and electric abnormalities.

Key points

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Gastroparesis is delayed gastric emptying in the absence of obstruction, a complication that affects patients with type 2 as well as type 1 diabetes mellitus.
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Symptoms associated with gastroparesis are nonspecific, and the diagnoses should be confirmed with gastric emptying tests.
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Patients are often overweight and have nutritional deficiencies.
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Obstructive gastroparesis, a subset of gastroparesis, is caused by pyloric dysfunction, and botulinum toxin A injections may be helpful.
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Trending postprandial glucose excursions with continuous glucose monitoring aids in the dosing and timing of insulin administration in diabetic patients with gastroparesis.

Introduction

When gastroparesis afflicts patients with type 1 diabetes mellitus (T1DM) or type 2 diabetes mellitus (T2DM), the consequences are particularly severe. Symptoms associated with gastroparesis, such as early satiety, prolonged fullness, nausea, and vomiting of undigested food, not only reduce the quality of life but also compound difficulties in controlling blood glucose levels.

Gastroparesis is defined as a delay in the emptying of ingested food in the absence of mechanical obstruction of the stomach or duodenum. Many patients with diabetes (as well as their physicians) do not appreciate that gastroparesis has developed. In diabetic patients with gastroparesis, ingested food is not emptied in a predictable period of time; thus, the anticipated nutrient absorption is not the reality. Consequently, the selected dose and timing of insulin therapy to control postprandial glucose may be inappropriate.

In many patients with gastroparesis, erratic postcibal glucose levels result in swings from hypoglycemia to severe hyperglycemia and even ketoacidosis. Hyperglycemia itself elicits gastric dysrhythmias and slows gastric emptying. Patients frequently are seen in emergency rooms for low glucose levels, severe hyperglycemia, or ketoacidosis. Gastroparesis as an underlying condition needs to be considered in these cases.

In addition to antinauseant and prokinetic drug therapies, patients with diabetic gastroparesis also need to change their diet and the timing and dosing of insulin to better match the slow emptying of ingested food. The epidemiology, pathophysiology, clinical presentation, diagnostic testing, and treatments for diabetic gastroparesis are reviewed in this article.

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