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Aetna Aetna
Clinical Policy Bulletin:
Gastric Pacing and Gastric Electrical Stimulation
Number: 0678


Policy

Aetna considers gastric pacing (gastric pacemaker) and gastric electrical stimulation medically necessary for the treatment of symptoms of nausea and vomiting from chronic gastroparesis that is refractory to medical management.

Aetna considers gastric pacing and gastric electrical stimulation experimental and investigational for all other indications including the following because their effectiveness for these indications has not been established (not an all-inclusive list):

  • As an initial treatment for gastroparesis
  • For treatment of diabetes mellitus in persons without gastroparesis
  • For the treatment of obesity.

See also CPB 0061 - Nutritional SupportCPB 0113 - Botulinum Toxin, and CPB 0396 - Gastrointestinal Function: Selected Tests.



Background

Gastroparesis is a chronic gastric motility disorder of diabetic (both type 1 and type 2 diabetes) or idiopathic etiology.  It is characterized by delayed gastric emptying of solid meals.  Patients with gastroparesis exhibit bloating, distension, nausea, and/or vomiting.  In severe and chronic cases, patients may suffer dehydration, poor nutritional status, and poor glycemic control (in diabetics).  Although gastroparesis is often associated with diabetes, it is also found in chronic pseudo-obstruction, connective tissue disorders, Parkinson disease, and psychological pathology.  Therapeutic options of gastroparesis include prokinetic agents such as metoclopramide, and anti-emetic agents such as metoclopramide, granisetron, or odansetron.  Patients with severe gastroparesis may require enteral or total parenteral nutrition.

Gastric pacing (gastric pacemaker) entails the use of a set of pacing wires attached to the stomach and an external electrical device that provides a low-frequency, high-energy stimulation to entrain the stomach at a rhythm of 3 cycles per minute.  However, the gastric pacemaker is cumbersome and problematic for chronic use because of external leads. 

Thus, a newer, implantable device (the Enterra Therapy System by Medtronic, Minneapolis, MN) was developed to provide gastric electrical stimulation (GES).  Unlike gastric pacing, the Enterra delivers a high-frequency (12 cycles per minute), low-energy stimulation to the stomach.  This stimulating frequency does not entrain the stomach, and therefore does not normalize gastric dysrhythmias; hence, the term GES is employed to differentiate between the Enterra and gastric pacing.

The Enterra System was designed to treat intractable nausea and vomiting secondary to gastroparesis.   Electrodes are implanted in the serosa of the stomach laparoscopically or during a laparotomy, and are connected to the pulse generator that is implanted in a subcutaneous pocket.  The Enterra Therapy System (Medtronic, Minneapolis, MN) is currently the only GES that has received approval from the U.S. Food and Drug Administration (FDA).  It was cleared by the FDA as a humanitarian use device.  Thus, the manufacturer was not required to submit the level of evidence that would be required to support a pre-market approval application.  The data presented to the FDA documenting the "probable benefit" of GES (Gastric Electrical Stimulation System) were based on a multi-center double-blind cross-over study (FDA, 2000), which included 33 patients with intractable idiopathic or diabetic gastroparesis.  In the initial phase of the study, all patients underwent implantation of the stimulator and were randomly assigned to stimulation-ON or stimulation-OFF for the first month, with cross-over to OFF and ON during the second month.  The baseline vomiting frequency was 47 episodes per month, which significantly declined in both ON and OFF groups to 23 to 29 episodes, respectively.  However, there were no significant differences in the number of vomiting episodes between the two groups, suggesting a placebo effect.  Thus, long-term results of GES must be validated in longer term randomized studies.  It is important to note that GES did not return gastric emptying to normal in the majority of the treated-patients. 

There exist preliminary data that suggested gastric pacing may be beneficial to patients with refractory gastroparesis.  Forster et al (2001) reported the findings of 25 patients who underwent gastric pacemaker placement.  Both the severity and frequency of nausea and vomiting improved significantly at 3 months and improvements were sustained for 12 months.  Gastric emptying time was also numerically faster over the 12-month period.  Three of the devices were removed and 1 patient died of causes unrelated to the pacemaker 10 months post-operatively.  The authors stated that after placement of the gastric pacemaker, patients rated significantly fewer symptoms and had a modest acceleration of gastric emptying.

Abell et al (2002) performed GES in 33 patients with intractable gastroparesis.  Patients were assessed 3, 5 and 12 months following permanent implantation.  These researchers reported that 97 % of patients experienced greater than 80 % reduction in nausea and vomiting.  For 24 patients who were followed for 1 year, the average weight gain was 5.5 % and 9 of 14 patients receiving enteral or parenteral nutrition were able to discontinue it.  The authors stated that while symptoms improved in the majority of patients following implantation of gastric stimulators, a properly randomized study is needed to ascertain the extent of a favorable placebo response. 

Bortolotti (2002) noted that there are currently 3 principal methods of GES: (i) gastric electrical pacing, (ii) high-frequency GES, and (iii) sequential neural electrical stimulation.  The first method aims to reset a regular slow-wave rhythm, but is unable to re-establish efficient contractions and a normal gastric emptying.  High-frequency GES, although inadequate to restore a normal gastric emptying, nevertheless strikingly improves the dyspeptic symptoms, such as nausea and vomiting, giving the patients a better quality of life and a more satisfactory nutritional status.  The last method, neural electrical gastric stimulation, consists of a microprocessor-controlled sequential activation of a series of annular electrodes which encircle the distal 2/3 of the stomach and induce propagated contractions resulting in a forceful emptying of the gastric content.  The latter method is the most promising, but it has so far only been tested in animals and would need to be tested in patients with gastroparesis before it can be used as a solution for this disease.  All the afore-mentioned clinical studies, however, are not controlled and nearly all were published in abstract form.  Thus, further controlled studies are needed to ascertain which of these techniques is more useful for the treatment of gastroparesis.  This is in agreement with Rabine and Barnett (2001) who considered gastric pacing as an experimental technique for the management of patients with gastroparesis.  Additionally, Smith and Ferris (2003) stated that gastric pacing offers promise for patients with medically refractory gastroparesis but awaits further investigation.  Furthermore, in a systematic review of evidence of therapies for gastroparesis, Jones and Maganti (2003) concluded that gastric neurostimulation improves symptoms of nausea and vomiting, but therapeutic gain beyond placebo has not been demonstrated.

Abell et al (2003) reported on a 2-phase clinical study of GES for gastroparesis: in the first phase, lasting 2 months, the investigators attempted to blind participants to stimulation.  In the first phase, 33 patients with gastroparesis (17 diabetic, 16 idiopathic) were randomized to stimulation either ON or OFF for 1 month, then crossed-over to the other mode for 1 month.  During the second uncontrolled phase of the study, all patients had their stimulator turned ON and were followed at 6 and 12 months.  The investigators reported that, during the first phase of the study, vomiting frequency was significantly less in the ON position, than in the off position, with weekly vomiting frequencies of 6.8 and 13.5 episodes, respectively (p < 0.05).  Total symptom score (mean sum of 6 symptoms, rated from 0 (absent) to 4 (severe) was also slightly less in the ON position than the OFF position, with scores of 12.5 + 1.0 and 13.9 + 1.1, respectively.  The investigators noted that 21 patients preferred the ON mode and 7 patients preferred the OFF mode.  An assessment by the National Institute for Clinical Excellence (NICE, 2004) commented that the results of this study are based on short-term follow-up of a small number of patients.  The assessment noted that one of the difficulties in interpreting the evidence on this procedure in this and other studies is the reliance on self-reported measures of symptom relief.   Furthermore, given the nature of the GES procedure, it is possible that patients experienced a placebo response.  The investigators reported that, during the second phase, there were significant improvements from baseline in weekly vomiting frequency, total symptom score, and measures of gastric emptying.  However, only 24 subjects included in this study were followed for 12 months, and gastric emptying data were available for only 20 subjects at 12 months. 

More recent studies have examined the effectiveness of gastric pacing in refractory gastroparesis.  These studies are limited by the lack of a control group, so that the effect of GES on gastroparesis can not be distinguished from the effects of the waxing and waning nature of these symptoms and the effects of concurrent interventions that the patient may be receiving for this condition.  Lin et al (2004) reported on the results of an uncontrolled study of GES in diabetic patients (n = 48) with refractory gastroparesis.  The investigators reported that, after application of high-frequency GES by a permanently implanted system, improvements were observed in upper gastrointestinal symptoms, health-related quality of life, nutritional status, glucose control, and hospitalizations.  van der Voort and colleagues (2005) reported improvements in symptom control and decreases in gastric retention (measured scintigraphically) after 12-months of continuous high-frequency/low-energy GES in a small group (n = 17) of insulin-dependent diabetic subjects suffering from drug-refractory gastroparesis.  The lack of a control group limits the strength of conclusions that can be drawn from these studies.

MaCallum et al (2005) reported on 12 month outcomes of GES in an uncontrolled study of a small group (n = 16) of subjects with post-surgical gastroparesis.  The investigators reported that, after application of GES, there was significant improvement in upper gastrointestinal symptoms, quality of life, nutritional status, and hospitalization requirements.  Lin et al (2005) reported significant reductions in the use of prokinetic/anti-emetic medications and the need for hospitalization after application of GES in an uncontrolled study of refractory gastroparetic patients (n = 37).  The authors also reported that subjects clinical and quality of life outcomes significantly improved after 1 year follow-up.  Other long-term uncontrolled studies include those of Oubre et al (2005) (46 month follow-up) and Cutts et al (2005) (3 year follow-up).

An assessment by the National Institute for Clinical Excellence (2004) concluded that "[c]urrent evidence on the safety and efficacy of gastroelectrical stimulation for gastroparesis does not appear adequate to support the use of this procedure without special arrangements for consent and for audit or research".  The assessment explained that “[c]urrent evidence on the efficacy of the procedure relates mainly to relief from nausea and vomiting, which occurs in some patients. There is little evidence that the procedure improves gastric emptying.”  The assessment reported that one of the difficulties in interpreting the evidence on this procedure is that most studies lack a comparision group, and rely on self-reported measures of symptom relief.

Evidence-based guidelines on gastroparesis from the American Gastroenterological Association (Parkman et al, 2004) state: “Gastric electric stimulation is an emerging therapy for refractory gastroparesis …. Studies to better evaluate the efficacy of gastric electric stimulation are ongoing.  As this type of treatment evolves, further delineation of the overall effectiveness, the type of patient who will likely respond, optimal electrode placement, and stimulus parameters should be explored.”

In a case series study, Filichia and Cendan (2008) assessed the response of transplant patients with gastroparesis to GES (Enterra therapy) and compared to non-transplant recipients.  A questionnaire consisting of 11 questions was administered to investigate symptoms.  Patients were asked to score these symptoms before and after surgery using a 0 to 5 Likert scale.  A total of 13 consecutive patients underwent placement of the Enterra device with a mean follow-up of 12 +/- 6.1 months.  Transplant recipients were as likely as diabetic or idiopathic patients to show improvements in symptoms of nausea, vomiting, as well as retching and prandial symptoms following Enterra therapy.  In fact, transplant patients reported improvement in appetite and bloating symptoms more frequently than diabetics (p = 0.055 and p = 0.037, respectively).  The authors concluded that post-transplantation gastroparesis responds to Enterra therapy as well as in patients with idiopathic or diabetic gastroparesis.  They stated that Enterra therapy should be prospectively investigated in this population of patients.

Obesity is a major health problem among adults in the United States.  It is also an increasing health concern among American children as well as adolescents.  Various methods are employed in the management of obesity.  One of the new approaches is gastric pacing, which is intended to induce early satiety through electrical stimulation of the gastric wall.  However, the effectiveness of this technique in treating obesity has not been established.  Buchwald and Buchwald (2002) considered gastric pacing as an experimental procedure for the management of morbid obesity.

An assessment of gastric pacing for obesity by the Swedish Council on Technology Assessment in Healthcare (SBU, 2004) found that "[t]here is insufficient scientific evidence on the short-term patient benefit of gastric pacing" for obesity, and that "[t]here is no scientific evidence on the long-term patient benefit of gastric pacing" for this indication.  The assessment concluded:

“Gastric pacing is still an experimental method and should be used only in scientific studies that have been approved by a research ethics committee.  Trials that include adequate control groups are very much needed.”

Yao et al (2005) stated that acute retrograde gastric pacing at a tachygastrial frequency results in a significant reduction of water and food intake and a delay in gastric emptying without inducing any unacceptable symptoms.  The investigators concluded that it is worthy to explore its therapeutic potential for obesity.  In a review on the potential role of new therapies in modifying cardiovascular risk in over-weight patients with metabolic risk factors, Jensen (2006) noted that surgically implanted gastric pacemaker systems that modulate vagus nerve activity and delay gastric emptying are under study.

Salvi et al (2009) reported their 2-year experience on gastric pacing in the treatment of morbid obesity.  From August 2005 to January 2006, a total of 4 patients (mean age of 44 years) underwent placement for implantable gastric stimulation (IGS) therapy.  The mean bone mass index (BMI) was 41.8, mean weight 117.2 kg.  The IGS was activated 30 days after implantation.  Fasting and post-prandial plasma ghrelin concentrations after a test meal were measured before and 1, 2, 3 and 6 months after implantation.  All procedures were successfully completed laparoscopically.  There were no major operative complications.  Post-operative course was uneventful in all cases.  One patient was lost to follow-up after 6 months.  Post-operative lead dislodgement and cutaneous decubitus occurred in another patient, making necessary the removing of the device.  For the remaining 2 patients, there was a significant weight loss (49 kg) in 1, while weight was unchanged in the other.  Plasma ghrelin concentrations were not correlated among patients.  The authors concluded that morbid obese patients can undergo IGS implantation by laparoscopy with minimal peri-operative complications.  Attention to technical details is essential.  In accordance with the manufacturer, these data demonstrated that gastric pacing is a safe procedure for selected patients supported by adequate psychological treatment, but outcome about weight loss should be evaluated among bigger trial.  According to these investigators, their experience with IGS didn't provide satisfactory results, thus discouraging them to carry on with the study.

In a prospective, randomized, placebo-controlled, double-blind, multi-center study, Shikora et al (2009) compared IGS therapy with a standard diet and behavioral therapy regimen in a group of class 2 and 3 obese subjects by evaluating the difference in the percentage of excess weight loss (EWL) between the control and treatment groups.  The primary endpoint was the percentage of EWL from baseline to 12 months after randomization.  A total of 190 subjects were enrolled in this study.  All patients underwent implantation with the implantable gastric stimulator and were randomized to one of the following two groups: (i) the control group (stimulation off) or (ii) treatment group (stimulation on).  Patients were evaluated on a monthly basis.  All individuals who enrolled in this study agreed to consume a diet with a 500-kcal/day deficit and to participate in monthly support group meetings.  The procedure resulted in no deaths and a low complication rate.  The primary endpoint of a difference in weight loss between the treatment and control groups was not met.  The control group lost 11.7 % +/- 16.9 % of excess weight and the treatment group lost 11.8 % +/- 17.6 % (p = 0.717) according to an intent-to-treat analysis.  The authors concluded that IGS as a surgical option for the treatment of morbid obesity is a less complex procedure than current bariatric operations.  However, the results of the present study do not support its application.  They stated that additional research is needed to understand the physiology and potential benefits of this therapy.

Policker and colleagues (2009) noted that the TANTALUS System (MetaCure Limited) is a minimally invasive implantable device for the treatment of type 2 diabetes (T2DM).  The system detects food intake by sensing gastric electrical variations and applies electrical stimulation to the gut synchronized to natural gastric activity.  It is commercially available in Europe and Israel and is in clinical trials in the United States.  It has been tested in 132 patients worldwide to date.  These researchers re-analyzed previously reported data from different studies.  This retrospective analysis of the type 2 diabetes sub-population analyzed the expected benefit and characterized the significance of baseline A1c in the determination of the expected clinical outcome.  From the total cohort of 132 patients implanted with the TANTALUS device in 10 different centers in Europe and the United States, these investigators identified 50 subjects (27 females, 23 males) who were obese with uncontrolled T2DM on a stable regime of oral medication for 3 months before implantation of the device.  This population had similar inclusion/exclusion criteria as well as treatment protocols and were all treated for at least 24 weeks.  The analysis was based on the A1c change compared to baseline.  Data after 24 weeks demonstrated a reduction in A1c in 80 % of the patients with average drop in A1c of 1.1 +/- 0.1 %.  The average weight loss was 5.5 +/- 0.7 kg.  The authors concluded that these findings suggested that the TANTALUS stimulation regime can improve glucose levels and induce moderate weight loss in obese T2DM patients.

In an European multi-center, open-label clinical study, Bohdjalian and associates (2009) prospectively investigated the potential effect of the TANTALUS system on glycemic control and weight in over-weight subjects with T2DM.  A total of 13 T2DM obese (7 females, 6 males, BMI of 37.2 +/- 1.0 kg/m(2), range of 30.4-44.0 kg/m(2)) subjects treated with oral anti-diabetic medications but with poor glycemic control (HbA1c greater than or equal to 7 %, range of 7.3 to 9.5 %) were implanted laparoscopically with the TANTALUS system.  Thirteen subjects that had completed 3 months of treatment showed a significant reduction in HbA1c from 8.0 +/- 0.2 % to 6.9 +/- 0.1 % (p < 0.05), whereas fasting blood glucose decreased from 175 +/- 6 mg/dL to 127 +/- 8 mg/dL (p < 0.05).  The glycemic improvement was accompanied by reduction in weight from 104.4 +/- 4.4 kg to 99.7 +/- 4.8 kg, and in waist circumference from 122.3 +/- 3.2 cm to 117.0 +/- 3.0 cm.  The authors concluded that interim results with the TANTALUS system suggest that this stimulation regime can potentially improve glucose levels and induce moderate weight loss in obese T2DM subjects on oral anti-diabetic therapy with poor glycemic control.  They stated that further evaluation is needed to ascertain if this effect is due to induced weight loss and/or due to direct signal-dependent mechanisms.

Thazhath et al (2013) noted that delayed gastric emptying affects a substantial proportion of patients with long-standing diabetes, and when associated with symptoms and/or disordered glycemic control, affects quality of life adversely.  Important clinic-pathological insights have recently been gained by the systematic analysis of gastric biopsies from patients with severe diabetic gastroparesis, which may stimulate the development of new therapies in the coming decade.  The authors stated that experience with prokinetic therapies and treatments, such as pyloric botulinum toxin injection and GES, has established that relief of symptoms does not correlate closely with acceleration of delayed gastric emptying, and that well-designed randomized controlled trials are essential to determine the effectiveness of emerging therapies.

 
CPT Codes / HCPCS Codes / ICD-9 Codes
CPT codes covered if selection criteria are met:
43647
43648
43881
43882
64590
64595
95980
95981
95982
ICD-9 codes covered if selection criteria are met:
536.3 Gastroparesis
ICD-9 codes not covered for indications listed in the CPB (not all-inclusive):
278.00 Obesity, unspecified
278.01 Morbid obesity
249.00 - 250.93 Diabetes mellitus
Other ICD-9 codes related to the CPB:
276.50 - 276.52 Volume depletion
278.02 Overweight
306.4 Psychological malfunction arising from mental factors, gastrointestinal
332.0 Paralysis agitans
332.1 Secondary Parkinsonism
564.89 Other functional disorders of intestine
710.0 - 710.9 Diffuse diseases of connective tissue
783.1 Abnormal weight gain
783.6 Polyphagia
787.01 Nausea with vomiting
787.02 Nausea alone
787.03 Vomiting alone
787.3 Flatulence, eructation, and gas pain


The above policy is based on the following references:

Gastric Pacing and Gastric Electrical Stimulation for Gastroparesis:

  1. Hocking MP, Vogel SB, Sninsky CA. Human gastric myoelectric activity and gastric emptying following gastric surgery and with pacing. Gastroenterology. 1992;103(6):1811-1816. 
  2. Kelly KA. Pacing the gut. Gastroenterology. 1992;103(6):1967-1968.
  3. Meidema BW, Sarr MG, Kelly KA. Pacing the human stomach. Surgery. 1992;111(2):143-150. 
  4. Rothstein RD, Alavi A, Reynolds JC. Electrogastrography in patients with gastroparesis and effect of long-term cisapride. Digestive Dis Sci. 1993;38(8):1518-1524.  
  5. Cullen JJ, Kelly KA. The future of intestinal pacing. Gastroenterology Clin North Am. 1994;23(2):391-402. 
  6. Lin ZY, McCallum RW, Schirmer BD, Chen JD. Effects of pacing parameters on entrainment of gastric slow waves in patients with gastroparesis. Am J Physiol. 1998;274(1 Pt 1):G186-G191.
  7. Hasler WL. The brute force approach to electrical stimulation of gastric emptying: A future treatment for refractory gastroparesis? Gastroenterology. 2000;111(3):456-460. 
  8. U.S. Food and Drug Administration (FDA), Center for Devices and Radiologic Health (CDRH). EnterraTM Therapy System (formerly named Gastric Electrical Stimulation (GES) System). Humanitarian Use Device Exemption H990014, Issued March 31, 2000. Rockville, MD: FDA; August 22, 2000. Available at: http://www.fda.gov/cdrh/ode/H990014sum.html. Accessed August 1, 2002.
  9. Forster J, Sarosiek I, Delcore R, et al. Gastric pacing is a new surgical treatment for gastroparesis. Am J Surg. 2001;182(6):676-681.
  10. Horowitz M, Su YC, Rayner CK, Jones KL. Gastroparesis: prevalence, clinical significance and treatment. Can J Gastroenterol. 2001;15(12):805-813.
  11. Rabine JC, Barnett JL. Management of the patient with gastroparesis. J Clin Gastroenterol. 2001;32(1):11-18.
  12. Bortolotti M. The "electrical way" to cure gastroparesis. Am J Gastroenterol. 2002;97(8):1874-1883.
  13. Abell TL, Van Cutsem E, Abrahamsson H, et al. Gastric electrical stimulation in intractable symptomatic gastroparesis. Digestion. 2002;66(4):204-212.
  14. Abell T, McCallum R, Hocking M, et al. Gastric electrical stimulation for medically refractory gastroparesis. Gastroenterology. 2003;125(2):421-428.
  15. Smith DS, Ferris CD. Current concepts in diabetic gastroparesis. Drugs. 2003;63(13):1339-1358.
  16. Jones MP, Maganti K. A systematic review of surgical therapy for gastroparesis. Am J Gastroenterol. 2003;98(10):2122-2129.
  17. Forster J, Sarosiek I, Lin Z, et al. Further experience with gastric stimulation to treat drug refractory gastroparesis. Am J Surg. 2003;186(6):690-695.
  18. Lin Z, Forster J, Sarosiek I, McCallum RW. Treatment of diabetic gastroparesis by high-frequency gastric electrical stimulation. Diabetes Care. 2004;27(5):1071-1076.
  19. Lin Z, Forster J, Sarosiek I, McCallum RW. Effect of high-frequency gastric electrical stimulation on gastric myoelectric activity in gastroparetic patients. Neurogastroenterol Motil. 2004;16(2):205-212.
  20. National Institute for Clinical Excellence (NICE). Gastroelectrical stimulation for gastroparesis. Interventional Procedure Guidance 103. London, UK: NICE; December 15, 2004. Available at: http://www.nice.org.uk/page.aspx?o=82715. Accessed October 26, 2005.
  21. Parkman HP, Hasler WL, Fisher RS. American Gastroenterological Association medical position statement: Diagnosis and treatment of gastroparesis. Gastroenterol. 2004;127(5):1589-1591.
  22. Lin Z, Forster J, Sarosiek I, McCallum RW. et al. Treatment of diabetic gastroparesis by high-frequency gastric electrical stimulation. Diabetes Care. 2004;27(5):1071-1076.
  23. McCallum R, Lin Z, Wetzel P, et al. Clinical response to gastric electrical stimulation in patients with postsurgical gastroparesis. Clin Gastroenterol Hepatol. 2005;3(1):49-54.
  24. van der Voort IR, Becker JC, Dietl KH, et al. Gastric electrical stimulation results in improved metabolic control in diabetic patients suffering from gastroparesis. Exp Clin Endocrinol Diabetes. 2005;113(1):38-42.
  25. Cutts TF, Luo J, Starkebaum W, Is gastric electrical stimulation superior to standard pharmacologic therapy in improving GI symptoms, healthcare resources, and long-term health care benefits? Neurogastroenterol Motil. 2005;17(1):35-43.
  26. Lin Z, McElhinney C, Sarosiek I, et al. Chronic gastric electrical stimulation for gastroparesis reduces the use of prokinetic and/or antiemetic medications and the need for hospitalizations. Dig Dis Sci. 2005;50(7):1328-1334.
  27. Oubre B, Luo J, Al-Juburi A, et al. Pilot study on gastric electrical stimulation on surgery-associated gastroparesis: Long-term outcome. South Med J. 2005;98(7):693-697.
  28. Moga C, Harstall C. Gastric electrical stimulation (Enterra Therapy System) for the treatment of gastroparesis. Health Technology Assessment Report No. 37. Edmonton, AB: Alberta Heritage Foundation for Medical Research; January 1, 2006. Available at: http://www.ahfmr.ab.ca/publications/. Accessed March 12, 2006.
  29. Ontario Ministry of Health and Long-Term Care, Medical Advisory Secretariat (MAS). Gastric electrical stimulation. Health Technology Policy Assessment. Toronto, ON: MAS; August 2006. Available at: http://www.health.gov.on.ca/english/providers/program/ohtac/tech/reviews/pdf/rev_ges_081806.pdf. Accessed October 12, 2007.
  30. Gourcerol G, Leblanc I, Leroi AM, et al. Gastric electrical stimulation in medically refractory nausea and vomiting. Eur J Gastroenterol Hepatol. 2007;19(1):29-35.
  31. Filichia LA, Cendan JC. Small case series of gastric stimulation for the management of transplant-induced gastroparesis. J Surg Res. 2008;148(1):90-93.
  32. McKenna D, Beverstein G, Reichelderfer M, et al. Gastric electrical stimulation is an effective and safe treatment for medically refractory gastroparesis. Surgery. 2008;144(4):566-572; discussion 572-574.
  33. Soffer E, Abell T, Lin Z, et al. Review article: Gastric electrical stimulation for gastroparesis -- physiological foundations, technical aspects and clinical implications. Aliment Pharmacol Ther. 2009;30(7):681-694.
  34. O'Grady G, Egbuji JU, Du P, et al. High-frequency gastric electrical stimulation for the treatment of gastroparesis: A meta-analysis. World J Surg. 2009;33(8):1693-1701.
  35. Yin J, Abell TD, McCallum RW, Chen JD. Gastric neuromodulation with enterra system for nausea and vomiting in patients with gastroparesis. Neuromodulation. 2012;15(3):224-231.
  36. Chu H, Lin Z, Zhong L, et al. Treatment of high-frequency gastric electrical stimulation for gastroparesis. J Gastroenterol Hepatol. 2012;27(6):1017-1026. 
  37. Camilleri M, Parkman HP, Shafi MA, et al. Clinical guideline: Management of gastroparesis. Am J Gastroenterol. 2013;108(1):18-37; quiz 38.

Gastric Pacing and Gastric Electrical Stimulation for Obesity and Diabetes:

  1. Deitel M, Shikora SA. Introduction. Gastric pacing for obesity. Obes Surg. 2002;12 Suppl 1:2S.
  2. Greenstein RJ, Belachew M. Implantable gastric stimulation (IGS) as therapy for human morbid obesity: Report from the 2001 IFSO symposium in Crete. Obes Surg. 2002;12 Suppl 1:3S-5S.
  3. Cigaina V. Gastric pacing as therapy for morbid obesity: Preliminary results. Obes Surg. 2002;12 Suppl 1:12S-16S.
  4. Buchwald H, Buchwald JN. Evolution of operative procedures for the management of morbid obesity 1950-2000. Obes Surg. 2002;12(5):705-717.
  5. Ouyang H, Yin J, Chen JD. Therapeutic potential of gastric electrical stimulation for obesity and its possible mechanisms: A preliminary canine study. Dig Dis Sci. 2003;48(4):698-705.
  6. Cigaina V, Hirschberg AL. Gastric pacing for morbid obesity: Plasma levels of gastrointestinal peptides and leptin. Obes Res. 2003;11(12):1456-1462.
  7. Swedish Council on Technology Assessment in Healthcare (SBU). Gastric pacing (gastric electrical stimulation) for the treatment of obesity -- early assessment briefs (Alert). Stockholm, Sweden: SBU; 2004.
  8. Cigaina V. Long-term follow-up of gastric stimulation for obesity: The Mestre 8-year experience. Obes Surg. 2004;14 Suppl 1:S14-S22.
  9. Liu S, Hou X, Chen JD. Et al. Therapeutic potential of duodenal electrical stimulation for obesity: Acute effects on gastric emptying and water intake. Am J Gastroenterol. 2005;100(4):792-796.
  10. Yao S, Ke M, Wang Z, et al. Retrograde gastric pacing reduces food intake and delays gastric emptying in humans: A potential therapy for obesity? Dig Dis Sci. 2005;50(9):1569-1575.
  11. Jensen MD. Potential role of new therapies in modifying cardiovascular risk in overweight patients with metabolic risk factors. Obesity (Silver Spring). 2006;14 Suppl 3:143S-149S.
  12. McNatt SS, Longhi JJ, Goldman CD, McFadden DW. Surgery for obesity: A review of the current state of the art and future directions. J Gastrointest Surg. 2007;11(3):377-397.
  13. Cigaina V, Hirschberg AL. Plasma ghrelin and gastric pacing in morbidly obese patients. Metabolism. 2007;56(8):1017-1021.
  14. Sanmiguel CP, Haddad W, Aviv R, et al. The TANTALUS system for obesity: Effect on gastric emptying of solids and ghrelin plasma levels. Obes Surg. 2007;17(11):1503-1509.
  15. Salvi PF, Brescia A, Cosenza UM, et al. Gastric pacing to treat morbid obesity: Two years experience in four patients. Ann Ital Chir. 2009;80(1):25-28.
  16. Shikora SA, Bergenstal R, Bessler M, et al. Implantable gastric stimulation for the treatment of clinically severe obesity: Results of the SHAPE trial. Surg Obes Relat Dis. 2009;5(1):31-37.
  17. Policker S, Haddad W, Yaniv I. Treatment of type 2 diabetes using meal-triggered gastric electrical stimulation. Isr Med Assoc J. 2009;11(4):206-208.
  18. Bohdjalian A, Ludvik B, Guerci B, et al. Improvement in glycemic control by gastric electrical stimulation (TANTALUS) in overweight subjects with type 2 diabetes. Surg Endosc. 2009;23(9):1955-1960.
  19. Ma J, Rayner CK, Jones KL, Horowitz M. Diabetic gastroparesis: Diagnosis and management. Drugs. 2009;69(8):971-986.
  20. Hasler WL. Methods of gastric electrical stimulation and pacing: A review of their benefits and mechanisms of action in gastroparesis and obesity. Neurogastroenterol Motil. 2009;21(3):229-243.
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  22. McCallum RW, Snape W, Brody F, et al. Gastric electrical stimulation with Enterra therapy improves symptoms from diabetic gastroparesis in a prospective study. Clin Gastroenterol Hepatol. 2010;8(11):947-954.
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Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering plan benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains only a partial, general description of plan or program benefits and does not constitute a contract. Aetna does not provide health care services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors in private practice and are neither employees nor agents of Aetna or its affiliates. Treating providers are solely responsible for medical advice and treatment of members. This Clinical Policy Bulletin may be updated and therefore is subject to change.
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