What You Should Know About Diabetic Gastroparesis
It has been estimated that neuropathy affects between 10 to 50 percent of patients with diabetes. Specifically, autonomic sensory neuropathy is associated with a number of clinical entities such as postural hypotension, cardiac arrhythmia, bladder dysfunction and gastrointestinal motility disturbance. Symptoms of gastrointestinal motility abnormalities can include nausea, vomiting, post-prandial fullness, early satiety, belching, bloating, erratic blood glucose levels, lack of appetite, gastro-esophageal reflux and spasms of the stomach wall. Symptoms can be mild to severe, depending on the chronicity of disease.
Gastric neuropathy secondary to diabetes was first described by Rundles in 1945. It became widely recognized after 1958 through the work of Kassander, who used the term gastroparesis diabeticorum or diabetic gastroparesis (DG). Today, we define this as a delay in gastric emptying in the absence of mechanical obstruction. Although it is thought to be an infrequent complication of diabetes, no true population-based studies have been identified for correlation. In fact, it has been estimated that gastroparesis affects about 50 percent of people with diabetes.
Current clinical understanding shows a strong correlation between DG and other complications such as peripheral neuropathy and functional microvascular disease that directly affect the foot. Identifying DG in your exam can help give you a more accurate view of a patient’s ability to heal from a procedure or wound.
What Researchers Have Noted About The Possible Etiology
Researchers have postulated multiple factors as the pathogenetic cause of DG. The prevailing thinking is that delayed gastric emptying is a manifestation of the autonomic neuropathy affecting the gastrointestinal tract. Rundles believed that the cause of DG was damage to the vagal tracts within the autonomic system.
The stomach is innervated by the sympathetic and parasympathetic divisions of the autonomic nervous system. Each system contains extrinsic and intrinsic autonomic nerve fibers. The extrinsic sympathetic fibers innervate the stomach through the celiac plexus whereas the parasympathetic fibers enter through the gastric branch of the vagus nerve.
Vagal autonomic neuropathy has been proposed because of its role in the reflexes that regulate gastric motility and emptying. The motility disturbances are strongly related to the presence of autonomic neuropathy and are similar to those observed in the vagotomized stomach. Both the proximal and distal portion of stomach are controlled by neural and hormonal mechanisms. Neural influences involve input from vagal (parasympathetic) and sympathetic fibers. Other pathogenetic mechanisms on this same pathway of dysfunction include persistent elevations of blood glucose, abnormalities in enteric hormones, and altered insulin/glucagons secretion.
To date, there has been little information about the natural history of DG. Researchers have established that acute changes in blood glucose concentrations affect gastric emptying as well as motor functions in other regions of the GI tract. The exact physiology of the role of hyperglycemia is complex. It is apparent now that hyperglycemia plays a central role in GI motility by reducing fundic tone, inhibiting antral pressure waves and inhibiting stimulated pressure waves.
Horowitz recognized in 1996 that acute changes in blood glucose concentrations have a major reversible influence on gastric motor and sensory function. He noted that the variations in blood glucose concentration have a major influence on neuromuscular function throughout the gastrointestinal tract. This study found that episodes of acute hyperglycemia slowed gastric emptying not only in candidates with diabetes, but also in those without diabetes.