Gastroparesis

Educational Objectives

The goal of this program is to improve the management of gastrointestinal motility disorders. After hearing and assimilating this program, the clinician will be better able to:

1. Interpret gastric emptying studies.
2. Treat gastroparesis.

Summary

Gastroparesis: symptomatic chronic stomach condition characterized by marked delayed gastric emptying without mechanical obstruction; prevalence — 3- to 4-times more common in women; etiology — idiopathic, 36%; diabetes mellitus (DM), 29%; postsurgical, 13%; in the remainder, a combination of factors (rheumatologic, central nervous system disorders, infections, medications)

Epidemiology: DM gastroparesis — patients with long-standing type 1 or 2 DM report nausea (≤30%) and recurrent vomiting (16%); ≤50% of patients with type 1 DM report delayed gastric emptying (≈50% of whom are symptomatic); associated with poor glycemic control; idiopathic gastroparesis — women comprise >80% of cases; healthy women demonstrate slower gastric emptying during the luteal phase of the menstrual cycle; postoperative gastroparesis — associated with selective vagotomy (≤5%); rates are higher with Roux-en-Y surgery, gastrojejunostomy, and Whipple procedures (≤50%); a large percentage of patients who have undergone lung and heart-lung transplantation demonstrate delayed emptying; most cases of postoperative gastroparesis are related to Nissen fundoplication (ie, stunning the vagus nerve)

Clinical features: nausea, vomiting, bloating, and early satiety; 50% to 80% of patients present with abdominal pain (possibly from another etiology); 10% to 40% of patients with gastroesophageal reflux disease demonstrate delayed gastric emptying; variable correlation with scintigraphy (ie, a slow gastric emptying study does not necessarily indicate severe symptoms); obesity affects the majority of patients; vitamin deficiency is not uncommon

Diagnosis: perform esophagogastroduodenoscopy to rule out gastric outlet obstruction or bezoar; a 4-hr solid-phase gastric emptying study with liquid egg whites and technetium is considered gold standard; order small bowel follow-through or computed tomography of the abdomen with oral and IV contrast to rule out postgastric mechanical obstructive process; laboratory testing — check thyrotropin, hemoglobin A1C, and autoimmune markers

Gastric emptying studies: follow scintigraphy curve out to 4 hr; anticipate ≥60% emptying at 120 min and 90% at 4 hr; slower times indicate gastroparesis

Pathophysiology: early satiety may relate more to accommodation by the stomach than to delayed emptying; use drugs to mimic excitatory neurotransmitters; avoid inhibitory neurotransmitters (eg, opioids) that slow gastric emptying; other causes — antral hypomotility; impaired fundic accommodation; hypertonic pylorus (DM); lack of coordination among multiple issues; gastric, sensory, or motor hypersensitivity in the enteric nervous system or vagus nerve; gastric myoelectrical dysrhythmia affecting interstitial cells of Cajal leads to disorganized contractility; postgastric etiology — slow small bowel or colon transit; autonomic neuropathy; inflammatory conditions; abnormalities in CNS centers for nausea and vomiting; medications — anticholinergic drugs; tricyclic antidepressants; calcium channel blockers; glucagon-like peptide (GLP)-1 agonists; opioids; tetrahydrocannabinol

Dietary modification: select liquids and low-fat foods; avoid red meat; choose low-fiber foods (avoid raw vegetables and salads); eat frequent, small meals; microparticle diet — validated for gastroparesis; drink foods that are liquified (ie, put through a blender); Olausson et al (2014) — reported improvements in nausea, vomiting, bloating, and postprandial fullness and reflux in diabetics with gastroparesis; glycemic control — hyperglycemia delays gastric emptying even in patients without DM

Pharmacologic Treatment

Antiemetic agents: act centrally; useful as adjunctive therapy; no evidence of efficacy for gastroparesis

Cannabinoids: used by 30% of patients with gastroparesis (those with the most severe disease)

Aprepitant: antiemetic; NK-1 receptor antagonist; very effective; Pasricha et al (2018) — reported that use reduced the severity of symptoms of gastroparesis

Prokinetic agents: metoclopramide — acts centrally and peripherally as a dopamine-receptor antagonist; antiemetic; has a black box warning for tardive dyskinesia; use can exacerbate depression and anxiety; domperidone — not approved by the US Food and Drug Administration (FDA); acts as a peripheral dopamine-2 receptor antagonist; observe for QT prolongation; cisapride — may be the best agent for gastric motility but associated with arrhythmia; erythromycin — acts as motilin-receptor agonist; drug holidays are needed; monitor QTc

Mirtazapine: atypical antidepressant; acts as an adrenergic, serotonergic, and histaminergic blocker; has weak prokinetic effects and strong antiemetic and gastric accommodation effects; stimulates appetite (monitor weight)

Tricyclic antidepressants: Parkman et al (2013) reported no reduction in symptoms for idiopathic gastroparesis after 15 wk; not a first-line drug for delayed gastric emptying

Prucalopride: now available in the United States; acts as a 5-HT4 receptor agonist; approved by the FDA for constipation; accelerates gastric emptying in gastroparesis; Carbone et al (2019) — reported improvement in symptoms in a small randomized trial

Ghrelin: endogenous peptide; stimulates gastric emptying; ghrelin agonists have shown benefit in randomized trials

Complementary therapy: ginger acts as a weak 5-HT3 receptor antagonist; acupuncture may help

Enteral feeding: place gastrojejunostomy or jejunostomy tubes; there is a risk for localized wound infection; avoid total parenteral nutrition (with at-home use, the sepsis rate is ≤14%; more expensive than feeding tubes)

Readings

Carbone F et al: Prucalopride in gastroparesis: A randomized placebo-controlled crossover study. Am J Gastroenterol, 2019 Aug;114(8):1265-74; Fosso CL, Quigley EMM: A critical review of the current clinical landscape of gastroparesis. Gastroenterol Hepatol (N Y), 2018 Mar;14(3):140-5; Olausson EA et al: A small particle size diet reduces upper gastrointestinal symptoms in patients with diabetic gastroparesis: A randomized controlled trial. Am J Gastroenterol, 2014 Mar;109(3):375-85; Parkman HP et al: Effect of nortriptyline on symptoms of idiopathic gastroparesis: The NORIG randomized clinical trial. JAMA, 2013 Dec;310(24):2640-9; Pasricha PJ et al: Aprepitant has mixed effects on nausea and reduces other symptoms in patients with gastroparesis and related disorders. Gastroenterology, 2018 Jan;154(1):65-76; Pasricha PJ, Parkman HP: Gastroparesis: Definitions and diagnosis. Gastroenterol Clin North Am, 2015 Mar;44(1):1-7.

Disclosures

For this program, members of the faculty and planning committee reported nothing to disclose. In his lectures, Dr. Bulat presents information related to the off-label or investigational use of a therapy, product, or device.

Acknowledgements

Dr. Bulat was recorded at the 37th Annual Medical & Surgical Gastroenterology: A Multidisciplinary Approach, held January 26-30, 2020, in Vail, CO, and presented by the Johns Hopkins University School of Medicine. For information about upcoming CME activities sponsored by the Johns Hopkins University School of Medicine, please visit: hopkinsCME.cloud-cme.com. The Audio Digest Foundation thanks the speakers and sponsors for their cooperation in the production of this program.

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

GE342102

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.