What You Should Know About Diabetic Gastroparesis

Pages: 16 - 18
By Jennifer Jansma, DPM, and John S. Steinberg, DPM

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. Key Diagnostic Indicators The diagnosis of DG is primarily a diagnosis of exclusion. The clinician must first eliminate the other possible causes of gastric dysfunction, including functional and mechanical obstruction. One can confirm DG through one or more of the following tests: barium X-ray, barium beefsteak meal, radioisotope gastric-emptying scan, upper GI endoscopy, ultrasound and gastric manometry. When you suspect DG, often one of the first signs you will notice is poor glycemic control. Asymptomatic patients may present with bezoar formation, unexplained hypoglycemic reactions, erratic absorption of oral medications, esophageal reflux and, rarely, even gastric bacterial overgrowth or candidiasis. Common symptomatic complaints include early satiety, anorexia, post-prandial fullness, nausea, vomiting, epigastric discomfort or pain, bloating, belching, heartburn, halitosis and weight loss. Severe cases of DG, if left untreated, can lead to nausea, vomiting, dehydration, malnutrition and ketoacidosis. Pertinent Pointers For Managing The Condition Once you have confirmed the diagnosis of DG, management consists of dietary and lifestyle modifications, glucose control, pharmacologic therapy and consideration of alternate feeding routes. The goal of treatment is to provide GI symptom relief, prevent the progression of neuropathy and enhance the quality of life. Glycemic control is very important in these patients because hyperglycemia can decrease gastric mobility, resulting in delayed gastric emptying. Some patients are able to improve by emphasizing good glycemic control and small, regular, frequent meals. Although the mainstay of treatment continues to be the use of pharmacological agents, there is strong evidence supporting the management of DG symptoms with prokinetic agents. Gastrokinetics, such as raglan, motilium and propulsid, stimulate gastric motility and promote more physiologic contraction in the stomach, pylorus, duodenum and small bowel. When it comes to the acutely ill patient with intractable symptoms, employing a feeding tube may be most beneficial. Using a jejunostomy tube allows the nutrients to bypass the stomach altogether. This method of treatment is particularly useful when severe gastroparesis prevents nutrient and medication absorption into the bloodstream. One may use jejunostomy feeding temporarily when gastroparesis is severe or it can be used permanently. Parenteral nutrition, an alternative approach to the jejunostomy tube, is usually a temporary method that is only used in cases of severe gastroparesis. An Early Glimpse At New Treatments In The Works There is hope through research and new treatments. One of those treatments under investigation is a gastric neurostimulator (“pacemaker”) that has been developed to assist in management of gastroparesis. It is a battery-operated, electronic device that is surgically implanted and emits mild electrical pulses that stimulate stomach contractions so food is digested and moved from the stomach into the intestines. This electrical stimulation has also been found to help control the nausea and vomiting associated with gastroparesis. Another new treatment uses botulinum toxin to decrease the prolonged contractions of the pyloric sphincter between the stomach and the small intestine. The toxin is injected into the pyloric sphincter and has early promise for stimulating gastric emptying. Final Notes There are multiple complications and symptoms that may arise from delayed gastric emptying. When this is left untreated, it can substantially impair the patient’s quality of life. There is also some concern that DG may be correlated with an increase in mortality among patients with diabetes. It is also well accepted that the presence of DG is a strong indicator of other advanced diabetic complications (nephropathy, retinopathy, functional microvascular disease and peripheral neuropathy). DG is a late manifestation of autonomic neuropathy and is associated with a poor prognosis. It is important to note that, in most cases, treatment does not cure gastroparesis. This is usually a chronic condition, but regaining control of blood glucose levels through treatment can help patients manage the condition and enhance their quality of life. Dr. Jansma is a first-year resident within the Department of Orthopaedics, Podiatry Division at the University of Texas Health Science Center in San Antonio, Texas. Dr. Steinberg (shown at the right) is an Assistant Professor within the Department of Orthopaedics, Podiatry Division at the University of Texas Health Science Center in San Antonio, Texas.



References 1. Tonzi MK, Fain JA. “Understanding Diabetic Gastroparesis, A Case Study.” Gastroenterology Nursing. Vol 25(4): 154-162. 2. Kong MF, Horowitz M, Jones KL, Wishart JM, Harding PE. “Natural History of Diabetic Gastroparesis.” Diabetes Care. March 1999,Vol 22 (3): 503-507. 3. Talley NJ. “Diabetic Gastropathy and Prokinetics.” American Journal of Gastroenterology. Vol 98 N2, 2003: 264-271. 4. Kockar MC, Kayahan IK, Bavbek N. Diabetic Gastroparesis in Association with Autonomic Neuropathy and Microvasculopathy. Acta Medica Okayama. Vol 56(5), May 2002. pp. 237-243. 5. Soewondo P. Gastoparesis in Diabetes: When to Suspect? Disampaikan pada Jakerta Diabetes Meeting 1999, 19-20. November 1999. 6. Vinik AI, Park TS, Stansberry KB, Pittenger GL. “Diabetic Neuropathies.” Diabetologia. Springer-Verlag 2000. pp:957-973. 7. Mayo Clinic Health Information, Mayo Foundation for Medical Education and Research, June 04, 2003. 8. National Digestive Diseases Information Clearinghouse (NDDIC), NIH Publication No. 03-4348. March 2003.



could the use of byetta cause this condition?

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