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Gastroparesis in Chronic Kidney Disease
- 1. Gastroparesis: An Overview VISHAL BAGCHI MBA, RD, LD DIRECTOR OF MEDICAL AND SCIENTIFIC AFFAIRS PATIENT CARE AMERICA
- 2. Disclaimer Employee of Patient Care America Non-FDA approved drugs are mentioned in this presentation 2
- 3. · Identify the common causes of gastroparesis in CKD · Overview of gut physiology · Differentiate gastroparesis vs. other GI issues and their symptoms · Provide comparison of gastroparesis & other common GI issues in CKD · Testing and findings · Compare and contrast various evidence- based treatments for gastroparesis · Review efficacy of current treatments in CKD for gastroparesis · Cite what providers can safely advise patients to reduce symptoms Objectives 3
- 4. History and Definition: Gastroparesis Objective evidence of delayed gastric emptying in absence of obstruction Symptoms: satiety, nausea, vomiting, bloating, and upper abdominal discomfort. It was first recognized as a complication of diabetes in 1945, and by 1958, the term "gastroparesis diabeticorum" was commonly used to describe the disorder. The primary cause for diabetic gastroparesis is thought to be related to autonomic neuropathy; however, virtually any disease or condition that can cause neuromuscular dysfunction of the GI tract 4 Park MI, Camilleri M. Gastroparesis: clinical update. Am J Gastroenterol. 2006;101:1129-1139
- 5. Stomach: Anatomy and Physiology Cardia and cardiac sphincter: prevents stomach contents from going back up into the esophagus. Body: Food is mixed and starts to break down. Pylorus: includes the pyloric sphincter muscle that acts as a valve to control the emptying of stomach contents (chyme) into the duodenum Bolus: Temporary storage held for 2 hours or longer Churning and Hydrolysis Pepsinogen + HCL = Pepsin Chyme: thick, acidic, soupy mixture 2-4L 5
- 6. Symptoms Defined Nausea: a subjective feeling of wanting to vomit, maybe referred by patients as indigestion or being full. Global sensation Vomiting: forceful expulsion of gastroduodenal contents Regurgitation: effortless expulsion of esophageal or gastric contents. Woke up middle of the night and was laying in vomit Retching: abdominal muscle contractions with labored rhythmic respiration. Nothing comes out Rumination: effortless regurgitation of recently ingested food, re- swallowing. Learned behavior 6 Images from Giphy
- 7. Etiologies of Gastroparesis 7 Idiopathic 36% Diabetic 29% Post-gastric surgery 13% Parkinson's disease 7.5% Collagen vascular disorders 4.8% Intestinal pseudo-obstruction 4.1% Miscellaneous causes 6% Etiologies of Gastroparesis in 146 Patients Seen in 1 Tertiary Referral Series. Soykan I, Sivri B, Sarosiek I, et al. Demography, clinical characteristics, psychological and abuse profiles, treatment, and long-term follow-up of patients with gastroparesis. Dig Dis Sci. 1998;43:2398-2404.
- 8. Gastric Emptying Study Standard: scintigraphy of solid phase meal Discontinue medications affecting gastric emptying for 48-72 hours Narcotics, anticholinergics delay emptying Metoclopramide, domperidone, erythromycin accelerate emptying Maintain normal glycemia Patients consume a standard low-fat meal labeled with 99mTc- sulfur colloid and are then imaged immediately after the meal is consumed, and at 1, 2, and 4 hours Results are reported as a percentage of gastric emptying at each time and compared to validated standard values Gastric emptying scintigraphy is available as an outpatient procedure only Wireless motility capsule Correlates 85% with T-90% emptying 13C octanoate breath tests Intraduodenal administration of 20 ml normal saline containing 100 mg 13C- octanoate and after ingestion of a 320-kcal muffin containing 100 mg 13C-octanoate 8 Article · Literature Review in European Journal of Clinical Investigation40(9):843-50 · September 2010 with 173 ReadsDOI: 10.1111/j.1365-2362.2010.02331.x · Source: PubMed
- 9. Normal Gastric Emptying Scintigraphy 9 J Neurogastroenterol Motil. 2011 Apr; 17(2): 189–191. Published online 2011 Apr 27. doi: 10.5056/jnm.2011.17.2.189
- 10. Delayed Gastric Emptying Scintigraphy 10 J Neurogastroenterol Motil. 2011 Apr; 17(2): 189–191. Published online 2011 Apr 27. doi: 10.5056/jnm.2011.17.2.189
- 11. Varied Gastric Emptying Time with the composition of the Meal 11 % Meal remaining in stomach Lag phase Emptying phase Time after meal (min) Solid meal Liquid meal 100 75 50 25 0 200 6040 10080 Semisolid meal
- 13. CKD Meds and Gastric Motility • Sevelamer is contraindicated in patients with bowel obstruction. • Considering that approximately two thirds of dialysis patients have some degree of dyspepsia-like symptoms, much of which may be related to overt or subclinical gastroparesis, these are important concerns. • For example, phosphate binding with calcium carbonate is optimal at a pH of approximately 5 while calcium acetate is effective through a broader pH range of 5 to 7 • This implies that calcium carbonate is most effective in the jejunum while calcium acetate is effective in both the jejunum and ileum. • Notably, neither agent is an effective phosphate binding agent at the low pH expected in the stomach where phosphorus is more easily bound to hydrogen than to calcium 13
- 14. Drugs that delay gastric emptying (Partial List) Gastrointestinal Agents Aluminum hydroxide Antacids H2 Receptor Antagonists (e.g. Ranitidine) Proton Pump Inhibitors (e.g. Omeprazole) Sucralfate- Treatment of Ulcers Ondansetron (Zofran) - N/V Anticholinergic Medications Diphenhydramine (Benadryl) Tricyclic Antidepressants Cardiovascular Medications Beta-Adrenergic Receptor Agonists Calcium Channel Blockers Diabetes Medications Incretin Mimetics (e.g. Exenatide, Liraglutide ) Pramlintide (Symlin) Miscellaneous Alcohol Opioid Analgesics Interferon alfa - Hepatitis Cyclosporine- immunosuppression Lithium 14
- 15. Mechanism of Gastroparesis *Not well studied but postulated • Fundal Hypomotility Different from fundoplication(Fundus stops working- Wrap the stomach around the esophagus) done for anti reflux surgery Solid phase delayed, liquid phase accelerated- Dumping Sx • Antral Hypomotility • Gastric arrhythmia • Lack of coordination 15
- 16. Evaluation Screen for: Diabetes mellitus (especially uncontrolled glucose levels) Thyroid dysfunction Neurological disease Prior gastric or bariatric surgery Autoimmune disorders Viral (post viral gastroparesis): Symptoms may improve over time Medication induced delay in gastric emptying: Narcotics, GLP-1 and amylin analogs, cyclosporine Confounding diagnoses: Cyclic vomiting syndrome, cannabinoid hyperemesis Rumination syndrome Eating disorders 16
- 17. Dietary Management of Gastroparesis Small frequent (6/day) meals Reduced fat (<40 gm/day) Soup, crackers, noodles, pasta, potatoes, rice, cheese Reduced fiber helps avoid bezoar a solid mass of indigestible material that accumulates in your digestive tract, sometimes causing a blockage Liquid caloric supplementation Glycemic control 17 Foods that are generally encouraged: • Breads, cereals, crackers, ground or pureed meats • Vegetables – cooked and, if necessary, blenderized/strained • Fruits – cooked and, if necessary, blenderized/strained • Juices, beverages, milk products, if tolerated • Small, frequent meals
- 18. High Fiber Foods/Medications Associated with Bezoar Formation – Avoid if possible Legumes/Dried Beans Bran /Whole Grain Cereals Nuts and Seeds Seeded Fruits Dried fruits Vegetables Foods Associated with Bezoar Formation Popcorn, Apples, Berries, Brussels sprouts, Coconuts, Corn, Figs, Green beans, Legumes, Oranges, Persimmons, Potato peels, Sauerkraut, Tomato skins High Fiber Medications/Bulking Agents Acacia fiber; Benefiber®; Citrucel®; FiberChoice®; Fibercon®; Konsyl®; Metamucil®; Perdiem Fiber, or any psyllium product 18 Carol Rees Parrish MS, RD and Nutrition Support Specialist University of Virginia Health and Jeanne Keith-Ferris, RN, BScN President/Founder, GPDA 5520 Dalhart Hill NW Calgary, AB T3A 1S9 https://uvahealth.com/services/digestive-health/images-and-docs/gastroparesis-diet.pdf
- 19. Wytiaz V et al, Dig Dis Sci 2015;60:1052-8 Provoking versus Alleviating Foods 19 Acidic, fatty, spicy, and fiber-rich foods provoke symptoms Bland, sweet, salty, and starchy foods alleviate symptoms
- 20. Dental Health • Since gastroparesis impairs the stomach’s ability to mash food and break it down into smaller sizes in preparation for absorption, the chewing of food beforehand becomes even more important. • In addition, repeated exposure to stomach acid from frequent vomiting may destroy tooth enamel. • Remind patients to see their dentist regularly and take good care of your teeth. • Perimylolysis, a smooth erosion of the tooth enamel, is common and manifests as a loss of enamel and eventually dentin on the lingual surfaces of the teeth caused by the chemical and mechanical effects of chronic regurgitation of low-pH gastric contents and movements of the tongue 20
- 21. Effect of dietary fat and food consistency on gastroparesis symptoms in patients with gastroparesis 21 Homko CJ et al, Neurogastroenterol Motil 2015;27:501-8
- 22. Low-fat liquid meal had the least effect Conclusions & Inferences • A high-fat solid meal significantly increased overall symptoms among individuals with gastroparesis, whereas a low-fat liquid meal had the least effect. • With respect to nausea, low-fat meals were better tolerated than high-fat meals, and liquid meals were better tolerated than solid meals. • These data provide support for recommendations that low-fat and increased liquid content meals are best tolerated in patients with symptomatic gastroparesis. *Can be difficult for patients on fluid restriction with dialysis 22 Homko CJ et al, Neurogastroenterol Motil 2015;27:501-8
- 23. Pro-kinetic and Anti-emetic Treatments 23 Friedenberg FK, Parkman HP. Clin Gastroenterol Hepatol 2005
- 24. Friedenberg FK, Parkman HP. Clin Gastroenterol Hepatol 2005 24
- 25. IDPN or IPN Intradialytic Amino Acids, Dextrose and Fat infusion 80-120 gm Amino Acids (80-90% absorption) 20-60 gm Dextrose 20-40 gm lipids 800-1200 kcal 400-700 mL volume 1000-1400 mOsm/l 3-4 hour infusion time Intraperitoneal Nutrition- Replacement of Dextrose bag with Amino Acids 30-60 gm Amino Acids (~80% Absorption) Patient Compliance Independent 25
- 26. Migrating motor complex (MMC) Phase I – A prolonged period of rest Phase II – Increased frequency of action potentials and smooth muscle contractility; Phase III – A few minutes of peak electrical and mechanical activity, and; Phase IV – Declining activity which merges with the next Phase I 26
- 28. Metoclopramide(Reglan) & Tardive Dyskinesia BLACK BOX WARNINGS: Metoclopramide can cause tardive dyskinesia (TD), a potentially irreversible and disfiguring disorder characterized by involuntary movements of the face, tongue, or extremities FDA APPROVAL: 1979 28
- 29. Prokinetics in Gastroparesis Dopamine-2 receptor antagonists metoclopramide(Reglan), domperidone (Motilium) Serotonin-4 receptor agonists cisapride, tegaserod (Zelnorm), prucalopride (Resolor- Canada) Motilin receptor agonists erythromycin Ghrelin receptor agonists ulimorelin (https://clinicaltrials.gov/ct2/show/NCT02784392) 29 Tack J et al, Curr Treatment Options Gastroenterol 2014;12:468-77
- 30. Interactive Question Which one of these agents have your patients been prescribed? Metoclopramide(Reglan) for 90 days or less Metoclopramide(Reglan) for greater then 90 days Erythromycin for 90 days or less Erythromycin for greater then 90 days Domperidone * expanded access IND I do not have any experience with these medications 30
- 31. Meta analysis: Effect of Medications on Symptom Improvement and Gastric Emptying 31 Janssens P et al, Am J Gastroenterol 2013;108:1382-91
- 32. Mirtazapine(Remeron) on gastrointestinal motility 32 Yin J et al, Am J Physiol 2014;306:G796-81 Mirtazapine accelerated gastric emptying in both normal dogs and delayed gastric emptying induced by rectal distension
- 33. Neuromodulators Improve Symptoms in Functional Nausea and Vomiting 33 Patel A, et al, Postgrad Med J 2013;89:131-6 Agents used: Tricyclic antidepressants-Pamelor etc SSRI- Lexapro, Zoloft etc SNRI- Cymbalta etc Zonisamide- Zonegran Levetiracetam- Keppra
- 34. Time trends in gastroparesis treatment 34 Shifted away from prokinetics > towards symptomatic management with antiemetics, and neuromodulators Dudekula A, et al. Dig Dis Sci. 2014.
- 35. Gastric Electrical Stimulation-Medtronic EnterraTM May consider for: Chronic vomiting Symptomatic disorders with abnormal gastric emptying Failure of medical therapy Non-narcotic based symptoms Candidate for abdominal surgery Evidence? Does not necessarily improve gastric emptying Not of value in cyclic vomiting 35 http://www.medtronic.com/us-en/patients/treatments-therapies/neurostimulator- gastroparesis/enterra-2-neurostimulator.html
- 36. Weekly vomiting frequency 36 Abell T, et al. Gastroenterology 2003
- 37. Gastric Stimulation placebo effect 37 McCallum RW et al, Clin Gastroenterol Hepatol 2010;8:947-54
- 38. Management of Symptoms 38 Adopted from: C. Prakash Gyawali, MD, MRCP Professor of Medicine Director, GI Fellowship Training Program Director, Neurogastroenterology and Motility Program
- 39. Take Home Message Gastric Emptying study gives you the best insight to validate gastroparesis and rule out anything else Nutrition and glycemic controls are the first line of defense Liquid and Semi-Solid small meals empty better vs solid meals Prokinetics and Neuromodulators may help patients alleviate symptoms but have varied results on gastric emptying 39
- 40. Questions? Vishal Bagchi MBA, RD, LD Director of Medical and Scientific Affairs Patient Care America vbagchi@pcacorp.com https://www.linkedin.com /in/vishalb3/ 40
- 41. Interactive Question Rank These By Ease Of Patient Compliance: 1=Easiest to comply with 5= Hardest to comply with • Small frequent (6/day) meals • Reduced fat (<40 gm/day) • Reduced fiber • Liquid caloric supplementation • Glycemic control 41
- 42. Nortriptyline (Pamelor) 42 Parkman H et al, JAMA 2013;310:2640-9
Editor's Notes
- Park MI, Camilleri M. Gastroparesis: clinical update. Am J Gastroenterol. 2006;101:1129-1139.
- 11
- Renagel [package insert]. Cambridge, Mass: Genzyme Corporation; 2004. Diabetic Patients With Gastroparesis and Chronic Kidney Disease -- Management of Malnutrition: An Expert Interview With William F. Finn, MD Authors:William Finn
- Different area of the stomach do not do what they are suppose to
- Approved GLP-1 agonists: exenatide (Byetta/Bydureon), approved in 2005/2012 liraglutide (Victoza, Saxenda), approved 2010[6] lixisenatide (Lyxumia), approved in 2016[7] albiglutide (Tanzeum), approved in 2014 by GSK[8] dulaglutide (Trulicity), approved in 2014—manufactured by Eli Lilly[9] semaglutide (Ozempic), approved in 2017.[10]
- Carol Rees Parrish MS, RD and Nutrition Support Specialist University of Virginia Health System Digestive Health Center of Excellence Charlottesville, VA President/Founder, GPDA 5520 Dalhart Hill NW Calgary, AB T3A 1S9 Legumes/Dried Beans (refried beans, baked beans, black-eyed peas, lentils, black, pinto, northern, fava, navy, kidney, garbanzo beans, soy beans) Bran /Whole Grain Cereals (such as bran cereals, Grape-Nuts®, shredded wheat type, granolas) Nuts and Seeds (pumpkin seeds, soy nuts, chunky nut butters) Fruits (blackberries, blueberries, raspberries, strawberries, oranges, kiwi) Dried fruits (apricots, dates, figs, prunes, raisins) Vegetables (green peas, broccoli) Foods Associated with Bezoar Formation Popcorn, Apples, Berries, Brussels sprouts, Coconuts, Corn, Figs, Green beans, Legumes, Oranges, Persimmons, Potato peels, Sauerkraut, Tomato skins High Fiber Medications/Bulking Agents Acacia fiber; Benefiber®; Citrucel®; FiberChoice®; Fibercon®; Konsyl®; Metamucil®; Perdiem Fiber, or any psyllium product
- Abstract Background Nutrition therapy for gastroparesis focuses on reducing meal size, fiber, fat intake, and increasing liquids intake relative to solid foods. Evidence to support these dietary interventions has been anecdotal. The aim of this study was to determine the effect of fat intake and solid/liquid meal consistency on symptoms in gastroparesis. Methods Twelve patients with gastroparesis were studied on four separate days receiving one of four meals each day in a randomized order: high-fat solid, high-fat liquid, low-fat liquid, and low-fat solid meal. At each visit, eight gastrointestinal symptoms were rated from 0 (none) to 4 (very severe) every 15 min, before and for 4 h after meal ingestion. Key Results There was an increase in the total symptom score in the following order: high-fat solid > low-fat solid > high-fat liquid > low-fat liquid. For the high-fat solid meal, symptoms remained elevated throughout the 4 h postprandial period. Severity of nausea more than doubled after the high-fat solid meal, whereas the low-fat liquid meal caused the least increase in nausea. Conclusions & Inferences A high-fat solid meal significantly increased overall symptoms among individuals with gastroparesis, whereas a low-fat liquid meal had the least effect. With respect to nausea, low-fat meals were better tolerated than high-fat meals, and liquid meals were better tolerated than solid meals. These data provide support for recommendations that low-fat and increased liquid content meals are best tolerated in patients with symptomatic gastroparesis.
- Neurogastroenterol Motil. 2015 Apr;27(4):501-8. doi: 10.1111/nmo.12519. Epub 2015 Jan 19. Effect of dietary fat and food consistency on gastroparesis symptoms in patients with gastroparesis. Homko CJ1, Duffy F, Friedenberg FK, Boden G, Parkman HP.
- Zelnorm – tegaserod not available
- The MMC originates mostly in the stomach—although ~25% will arise from the duodenum or proximal jejunum—and can travel to the distal end of the ileum.[3] They consist of four distinct phases: Boron, Walter F.; et, al, eds. (2012). Medical physiology : a cellular and molecular approach(Updated second ed.). Philadelphia, Pa.: Saunders. ISBN 978-1437717532.
- Designed in 1970’s convert any phase of MMC to phase 3 MMC emptying undigested emptying into intestines. Reglan induces that even if you have just eaten- Causing mostly likely causing diarrhea. Small intestine is not ready. GI Bleed - IV Reglan Keep giving it, effect goes away. Works like a neuro modulators,
- In the United States, domperidone is not currently a legally marketed human drug and it is not approved for sale in the U.S. On 7 June 2004, FDA issued a public warning that distributing any domperidone-containing products is illegal.[12] It was reported in 2007 that domperidone is available in 58 countries, including Canada,[10] but the uses or indications of domperidone vary between nations. In Italy it is used in the treatment of gastroesophageal reflux disease and in Canada, the drug is indicated in upper gastrointestinal motility disorders and to prevent gastrointestinal symptoms associated with the use of dopamine agonist antiparkinsonian agents.[11] In the United Kingdom, domperidone is only indicated for the treatment of nausea and vomiting and the treatment duration is usually limited to 1 week. Cisapride is only available in the United States to special patients who are signed up by their doctors. Talk to your doctor or pharmacist about whether you should be taking cisapride. Cisapride may cause serious irregular heart beats On March 30, 2007, the FDA asked Novartis to suspend its U.S. marketing and sales because a safety analysis found a higher chance of heart attack, stroke, and unstable angina (heart/chest pain) in patients treated with Zelnorm compared with treatment with an inactive substance (placebo). Prucalopride was approved for use in Europe in 2009,[8] in Canada in 2011[9] and in Israel in 2014[10] but it has not been approved by the Food and Drug Administration for use in the United States.
- relationship between symptom improvement (SI) and acceleration of gastric emptying (GE) metoclopramide (n=6), domperidone (n=6), cisapride (n=14), erythromycin (n=3), botulinum toxin (n=2), and levosulpiride (n=3). The relation between symptom improvement and gastric emptying in the treatment of diabetic and idiopathic gastroparesis. Janssen P1, Harris MS, Jones M, Masaoka T, Farré R, Törnblom H, Van Oudenhove L, Simrén M, Tack J.
- The Food and Drug Administration (FDA) approved these cyclic antidepressants to treat depression: Tricyclic antidepressants: Amitriptyline Amoxapine Desipramine (Norpramin) Doxepin Imipramine (Tofranil) Nortriptyline (Pamelor) Protriptyline (Vivactil) Trimipramine (Surmontil) The Food and Drug Administration (FDA) has approved these SSRIs to treat depression: Citalopram (Celexa) Escitalopram (Lexapro) Fluoxetine (Prozac) Paroxetine (Paxil, Pexeva) Sertraline (Zoloft) Vilazodone (Viibryd) The Food and Drug Administration (FDA) has approved these SNRIs to treat depression: Desvenlafaxine (Pristiq, Khedezla) Duloxetine (Cymbalta) ― also approved to treat anxiety and certain types of chronic pain Levomilnacipran (Fetzima) Venlafaxine (Effexor XR) ― also approved to treat anxiety and panic disorder
- Ondansetron –Zofran Dudekula A, et al. Dig Dis Sci. 2014. Show full citation Abstract INTRODUCTION: While delayed emptying is the defining criterion for gastroparesis, prokinetics often only have a limited impact on symptoms and have been associated with potentially serious adverse effects. The goal of this study was to determine how this information and regulatory changes affected gastroparesis management. METHODS: The electronic medical records of patients seen between 2003 and 2012 in the outpatient clinic of a large tertiary center were retrieved based on the billing diagnosis of gastroparesis. Demographic, clinical, and survival data were abstracted. RESULTS: A total of 709 patients were identified, with diabetes (21.2 %) and prior surgery (9.8 %) being the most common identifiable causes. The majority of patients (56 %) had idiopathic gastroparesis. The cohort was female predominant (79.5 %) with an average age of 45.4 ± 0.6 years. At the index encounter, 61.8 % received prokinetics. About one-third (37.7 %) used antiemetics at least intermittently. Between 2003 and 2012, prokinetic use dropped from 81 to 43 %, while the use of antiemetics increased from 14 to 41 %. Similarly, there was a significant increase in prescribed opioids and antidepressants. During the period of the study, 44 patients (6.2 %) died. Increasing age, a higher comorbidity burden, anxiety, and medication use were associated with higher mortality risks. CONCLUSION: This large outpatient cohort suggests that treatment trends move away from prokinetics and focus on symptom-oriented therapy and/or confounding mood disorders.
- Weekly vomiting frequency (median and interquartile range). The bar graph illustrates the changes in weekly vomiting frequency as recorded in patient diaries at baseline, during the ON and OFF periods of the double-blind phase, and at 6 and 12 months during the open-label phase. Diabetic: baseline, n = 17; ON, n = 17; OFF, n = 17; 6 months, n = 13; 12 months, n = 11. Idiopathic: baseline, n = 16; ON, n = 16; OFF, n = 16; 6 months, n = 14; 12 months, n =13. (†P < 0.05, ON vs. OFF; ∗P < 0.05 vs. baseline; ∗∗P< 0.05 vs. OFF). Gastric electrical stimulation for medically refractory gastroparesis☆ Thomas Abell , Richard McCallumCorrespondence information about the author Richard McCallumEmail the author Richard McCallum , Michael Hocking , Kenneth Koch , Hasse Abrahamsson , Isabelle LeBlanc , Greger Lindberg , Jan Konturek , Thomas Nowak , Eammon M.M Quigley , Gervais Tougas , Warren Starkebaum Methods: Thirty-three patients with chronic gastroparesis (17 diabetic and 16 idiopathic) received continuous high-frequency/low-energy gastric electrical stimulation via electrodes in the muscle wall of the antrum connected to a neurostimulator in an abdominal wall pocket. After implantation, patients were randomized in a double-blind crossover design to stimulation ON or OFF for 1-month periods. The blind was then broken, and all patients were programmed to stimulation ON and evaluated at 6 and 12 months. Outcome measures were vomiting frequency, preference for ON or OFF, upper gastrointestinal tract symptoms, quality of life, gastric emptying, and adverse events. Results: In the double-blind portion of the study, self-reported vomiting frequency was significantly reduced in the ON vs. OFF period (P < 0.05) and this symptomatic improvement was consistent with the significant patient preference (P < 0.05) for the ON vs. OFF period determined before breaking the blind. In the unblinded portion of the study, vomiting frequency decreased significantly (P < 0.05) at 6 and 12 months. Scores for symptom severity and quality of life significantly improved (P < 0.05) at 6 and 12 months, whereas gastric emptying was only modestly accelerated. Five patients had their gastric electrical stimulation system explanted or revised because of infection or other complications. Conclusions: High-frequency/low-energy gastric electrical stimulation significantly decreased vomiting frequency and gastrointestinal symptoms and improved quality of life in patients with severe gastroparesis.
- Summary Gastroparesis and functional dyspepsia can be indistinguishable by clinical presentation Delayed gastric emptying is the basis of diagnosis of gastroparesis, but can be also be encountered in functional dyspepsia Interest has shifted towards symptom based management approaches over prokinetic therapy Neuromodulators and gastric electrical stimulation are options in refractory states
- Identified Gap(s): Limited knowledge of gastroparesis etiology and treatment options by Dietitians and other practitioners. Description of current state: ESRD patients are commonly affected by gastroparesis and practitioners often have a limited understanding of scientifically proven therapies to improve patient outcomes, reduce hospitalizations, and improve quality of life. Description of desired/achievable state: Increased knowledge of scientifically based interventions for gastroparesis Gap to be addressed by this activity: Dietitians’ lack of comfort in making sound recommendations for patients with gastroparesis Activity Overview: The purpose of this activity is to enable the learner to identify the common causes of gastroparesis in CKD, differentiate gastroparesis vs other GI issues and their symptoms, and compare and contrast various evidence-based treatments for gastroparesis, and recognize three take-home strategies to offer patients/physicians..
- 130 patients with idiopathic gastroparesis from 7 centers Abnormal gastric emptying study, and GCSI score >21 required for enrollment Equally randomized to nortriptyline and placebo Gastroparesis Cardinal Symptom Index (GCSI): development and validation of a patient reported assessment of severity of gastroparesis symptoms. Gastroparesis Cardinal Symptom Index (GCSI): development and validation of a patient reported assessment of severity of gastroparesis symptoms. Revicki DA1, Rentz AM, Dubois D, Kahrilas P, Stanghellini V, Talley NJ, Tack J. Author information Abstract BACKGROUND: Patient-rated symptom assessments are needed for evaluating the effectiveness of medical treatments and for monitoring outcomes in gastroparesis. OBJECTIVE: This paper summarizes the development and psychometric evaluation of a new instrument, the Gastroparesis Cardinal Symptom Index (GCSI), for assessing severity of symptoms associated with gastroparesis. METHODS: The GCSI was based on reviews of the medical literature, patient focus groups, and interviews with clinicians. A sample of 169 patients with a documented diagnosis of gastroparesis participated in the psychometric evaluation study. Patients completed the GCSI, the SF-36 Health Survey, and disability days questions at baseline and after 8 weeks. A randomly selected sub-sample of 30 subjects returned at 2 weeks to assess test retest reliability. Clinicians rated severity of symptoms, and both clinicians and patients rated change in gastroparesis-related symptoms over the 8 week study. RESULTS: The GCSI is based on three subscales: post-prandial fullness/early satiety (4 items); nausea/vomiting (3 items), and bloating (2 items). Internal consistency reliability was 0.84 for the GCSI total score and ranged from 0.83 to 0.85 for the subscale scores. Two week test retest reliability was 0.76 for the total score and ranged from 0.68 to 0.81 for subscale scores. Construct validity was supported, given that we observed significant relationships between clinician assessed symptom severity and GCSI total score, significant differences between gastroparesis and dyspepsia patients (n = 760) on GCSI total (p < 0.0001) and subscale scores (p < 0.03 to p < 0.0001), moderate and significant relationships between GCSI total and SF-36 scores, and significant associations between GCSI total score and reports of restricted activity and bed disability days. Patients with greater symptom severity, as rated by clinicians, reported more symptom severity on GCSI total score. GSCI total scores were responsive to changes in overall gastroparesis symptoms as assessed by clinicians (p < 0.0001) and patients (p = 0.0004).