Diabetic Autonomic Neuropathy

Aaron I. Vinik, MD, PhD.; Roy Freeman, MB, ChB.; Tomris Erbas, MD

Disclosures

Semin Neurol. 2003;23(4) 

In This Article

Gastrointestinal Autonomic Neuropathy

Gastrointestinal symptoms are relatively common among patients with diabetes and often reflect diabetic gastrointestinal autonomic neuropathy. The prevalence of symptoms caused by gastrointestinal dysfunction may reach 76% in a nonselected population of diabetic outpatients.[37] Esophageal dysfunction results at least in part from vagal neuropathy; symptoms include heartburn and dysphagia for solids. Esophageal dysfunction is detectable through esophageal motility testing and esophageal scintigraphy in diabetic patients. Diabetic autonomic neuropathy can impair both gastric acid secretion and gastrointestinal motility, causing gastroparesis diabeticorum, which can be detected in 50% of patients with diabetes.[38] Gastric emptying largely depends on vagus nerve function, which can be severely disrupted in diabetes. Dysfunction of intrinsic enteric neurons may contribute as well. Major clinical features of this disorder are early satiety, anorexia, nausea, vomiting, epigastric discomfort, and bloating. Episodes of nausea or vomiting may last days to months or may occur in cycles. Patients with gastroparesis have emesis of undigested food consumed many hours or even days previously. The finding of retained food in the stomach after an 8- to 12-hour fast in the absence of obstruction is diagnostic of gastroparesis. Gastroparesis is also associated with the development of bezoars. Even with mild symptoms, gastroparesis interferes with nutrient delivery to the small bowel and therefore disrupts the relationship between glucose absorption and exogenous insulin administration. This can result in wide swings of glucose levels and unexpected episodes of postprandial hypoglycemia and apparent "brittle diabetes." Therefore, gastroparesis should be suspected in patients with erratic glucose control.[39] Gastric emptying can be visualized by scintigraphic imaging after the patient consumes radionuclide-labeled food, but the scintigraphic results do not always correlate with the severity of the symptoms. Hyperglycemia exerts a major influence on gastric motor function in that it slows gastric emptying in diabetic patients.

Diarrhea and other lower gastrointestinal tract symptoms may also occur. Diabetic diarrhea manifests as a profuse, watery, typically nocturnal diarrhea, which can last for hours or days and frequently alternates with constipation. Abdominal discomfort is commonly associated. The pathogenesis of diabetic diarrhea includes reduced gastrointestinal motility, reduced receptor mediated fluid absorption, bacterial overgrowth, pancreatic insufficiency, coexistent celiac disease, and abnormalities in bile salt metabolism.[40] Fecal incontinence due to anal sphincter incompetence or reduced rectal sensation is another manifestation of diabetic gastrointestinal neuropathy. The most common problem associated with diabetic gastrointestinal dysfunction is constipation, affecting nearly 60% of diabetic patients. Severe constipation may be complicated by perforation and fecal impaction.

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