Diabetic gastroparesis
Bloating is often a sign of this little-known complication
by Netee Papneja, MD and Ally P.H. Prebtani, MD
Vol.19, No.05, June 2011

Diabetic Gastroparesis (DGP) is characterized by delayed gastric emptying in the absence of a mechanical obstruction.1 Approximately 5-12% of diabetics have gastroparesis, with a higher prevalence in females, type 1 disease, those with long-standing type 2 DM, poor glycemic control, and in the presence of microvascular complications.1-3 DGP is mainly due to autonomic neuropathy. It’s also associated with acute hyperglycemia, the use of incretin-based therapies, and psychosomatic factors.4-7

The predominant symptoms of gastroparesis are post-prandial fullness, early satiety, nausea, vomiting and/or bloating.8 Abdominal discomfort or pain can also occur in 46% to 89% of patients, but it’s rarely the chief complaint.9 The symptoms are variable; however, the strongest predictors of DGP are postprandial fullness and bloating.3 Symptom severity, though, is poorly correlated with the degree of gastric emptying.3 DGP can also lead to poor and labile glycemic control (both hyper- and hypoglycemia) because of meal unpredictability, abnormal absorption and gastric emptying, and vomiting. In these cases, rapid acting insulin analogues given after meals may be more effective and safer than regular insulin.

The diagnosis of DGP is based upon exclusion of other causes of gastroparesis (Table 1) and objective evidence of delayed gastric emptying in a symptomatic patient.1 The diagnostic approach to gastroparesis recommended by the American Gastroenterological Association (see flow chart) consists of an initial evaluation with a patient history and physical examination followed by laboratory investigations.1 If these fail to yield a diagnosis, then most patients will get upper endoscopy or barium radiography to exclude an obstruction. If a patient has biliary tract symptoms or significant abdominal pain, ultrasonography or abdominal radiographs should be considered.1 Scintigraphic measurement of gastric emptying is recommended to confirm the diagnosis of gastroparesis.1

Table 1 Differential diagnosis of gastroparesis

The management of DGP consists of supportive measures, optimizing glycemic control, pharmacological therapy, stopping any offending medications, and occasionally invasive therapy. Patients with delayed gastric emptying can have modest clinical benefit from a low fat and fibre diet, and small frequent liquid-based meals. Hydration and nutrition are essential if vomiting is an issue. Enteral or parenteral feeding may be needed in severe cases of DGP with inadequate oral intake, malnutrition, weight loss, and frequent hospitalizations.

The mainstay of pharmacological therapy for DGP involves prokinetic medications such as domperidone, metoclopramide, and erythromycin (see table 2 for comparison www.parkhurstexchange.com/columns/diabetes/june11_flow-chart-and-table2#table2).10 If symptoms of nausea and vomiting are present then anti-emetic drugs such as dimenhydrinate, prochlorperazine, and ondansetron can be added. Management of refractory gastroparesis should be done along with a gastroenterologist for assessment of more invasive alternatives such as intrapyloric botulinum toxin injections, placement of a jejunostomy tube, or implantation of a gastric stimulator/pacer. Furthermore, several new therapeutic strategies for gastroparesis are currently being investigated including prokinetic agents such as 5-hydroxytryptamine agonists, ghrelin agonists, and stem cell therapies.11-13

In summary, DGP is a frequent complication of DM and can have deleterious effects on quality of life. The evidence for therapy in DGP is suboptimal and is an area that needs further, higher-quality research.

References

  1. Parkman HP, et al. Gastroenterology 2004;127(5):1592-622.
  2. Keshavarzian A, et al. Am J Gastroenterol 1987;82:29-35.
  3. Jones KL, et al. Diabetes Care 2001;24:1264-9.
  4. Horowitz M, et al. Diabet Med 1996;13(Suppl 5):S16-22.
  5. Camilleri M. Clin Gastroenterol Hepatol 2009;7:285-7.
  6. Lustman PJ, Clouse RE. J Diabetes Complications 2005;19:113-22.
  7. Rayner CK, et al. Diabetes Care 2001;19:371-81 (Review).
  8. Revicki DA, et al. Aliment Pharmacol Ther 2003;18:141-50.
  9. Hoogerwerf WA, et al. Am J Gastroenterol 1999;Apr;94(4):1029-33.
  10. Samsom M, et al. Gastroenterol Int 1998;19:169-76.
  11. Melga P, et al. Diabetes Care 1997;19:55-8.
  12. Tougas G, Huizinga JD. Gastroenterology 1998;19:598-601.
  13. Gaber AO, et al. Dig Dis 1991;19:437-43.
  14. Patterson D, et al. Am J Gastroenterol 1999;94:1230-4.
  15. Rao AS, Camilleri M. Aliment Pharmacol Ther 2010;31:11-9.
  16. Maganti K, et al. Am J Gastroenterol 2003;98(2):259.

Netee Papneja, MD, is a medical resident at McMaster University.

Ally P.H. Prebtani, MD, FRCPC, is Associate Professor of Medicine and Program Director of the Endocrinology & Metabolism Residency Training Program at McMaster University in Hamilton, ON. He is also Director of the Internal Medicine International Health Program at McMaster.

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(photo: ENE/Shutterstock.com)
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