February 2025 Issue

CPE Monthly: Gastroparesis: An Update
By Lauren Botelho, MS, RD, LDN
Today’s Dietitian
Vol. 27 No. 2 P. 26

Take this course and earn 2 CEUs on our Continuing Education Learning Library

Gastroparesis, also known as gastric stasis, is a disorder in which there is delayed gastric emptying without mechanical obstruction.1 To further understand gastroparesis, it is important to first look at how digestion occurs. The stomach is an organ within the digestive system. It contains three muscle layers: the circular, oblique, and longitudinal layers. It has the ability to store meals, grind up solid food, and pump ground-up food/liquid into the small intestine via muscular contractions.2 An anatomic sphincter is formed at the pylorus via thickening of the circular layer. Complex grinding is the result of the oblique layer. The “gastric pacemaker” is found in the midportion of the greater curvature. Pacer cells that are involved in electrical coupling with neighboring cells cause electrical activity and contractility to occur. The stomach’s ability for contractility can be changed by many different stimuli and conditions.1

Gastroparesis occurs when the stomach’s muscular contractions are impaired, causing a delay in the emptying of the stomach’s contents. Gastroparesislike symptoms have been found in an estimated 4% of the population, although the exact number of people suffering from gastroparesis is unknown. However, it is suggested that more than 1.5 million Americans suffer from severe gastroparesis. It can begin at any age, with the most common age of onset being 34. It is more commonly seen in women. In fact, 80% of those with gastroparesis are women.2

This continuing education course examines the etiology, symptoms, and treatment of gastroparesis. It explains the role of the care team in utilizing MNT and nutrition support for gastroparesis.

Types of Gastroparesis
Gastroparesis results from many different diseases/disorders. Common causes include uncontrolled diabetes, postviral effects, connective tissue diseases (such as multiple sclerosis, muscular dystrophy, amyloidosis, scleroderma), side effects from medications (such as narcotics, tricyclic antidepressants, calcium channel blockers, progesterone, anticholinergic drugs), postsurgical effects (eg, damage to the vagus nerve following a gastrointestinal [GI] surgery), radiation therapy, cancer, hypothyroidism, eating disorders, and chemotherapy. These causes are risk factors for developing the disorder, even if symptoms are not currently present. The ultimate cause of this disorder is due to damage to the peripheral nerves and muscles.3

Diabetes and Gastroparesis
Gastroparesis is extremely common in those with diabetes. However, the exact number of those affected is questionable. Some research suggests that 11% to 18% of patients with diabetes have been found to have upper GI symptoms and 50% to 65% of these patients have been found to have gastroparesis when examined. Furthermore, some studies show that gastroparesis has been reported in 30% to 50% of patients with type 1 diabetes and 15% to 30% of those with type 2 diabetes.4 Other statistics show that 40% of people with type 1 diabetes have gastroparesis and 30% of those with type 2 have it.5 In these patients, gastroparesis typically results from nerve damage caused by poor glucose control rather than muscle damage.3

In people living with diabetes, the vagus nerve can become damaged over time due to hyperglycemia. Blood vessels deliver oxygen and nutrients to nerves. Nerves are bundles of different types of tissues that enable signals to cross between the brain and other body parts; they help control digestion.6 Over time, high blood glucose levels can cause chemical changes in nerves and damage to blood vessels.5 This type of damage is called autonomic neuropathy.6

There are several risk factors for neuropathy in those with diabetes. These include being overweight, having high blood pressure, having high cholesterol, having advanced kidney disease, overconsumption of alcohol, and smoking. In addition to hyperglycemia being a main cause of diabetic neuropathy, high triglyceride levels can contribute as well, leading to nerve damage. Nerves become deprived of adequate oxygen and nutrients, causing a decrease in function.6

Idiopathic Gastroparesis
Another common form of gastroparesis is idiopathic gastroparesis, which has an unknown cause. This form of gastroparesis does not result from diabetes or gastric surgery. It is unrelated to endocrine, neurologic, or rheumatologic causes or medications that could cause gastroparesis. Some of the symptoms can overlap with dyspepsia, and some patients may have both functional dyspepsia and gastroparesis. Due to the similarities in symptoms shared by both dyspepsia and gastroparesis, it may be difficult to diagnose and distinguish between the two. Although most forms of gastroparesis display similar symptoms, idiopathic gastroparesis tends to more commonly cause abdominal pain vs diabetic gastroparesis. Nausea and vomiting tend to be more severe in diabetic gastroparesis.7

Per the Rochester Epidemiology Project, “definite” gastroparesis is defined as a diagnosis of “delayed gastric emptying by standard scintigraphy, symptoms of nausea and/or vomiting, postprandial fullness, early satiety, bloating, or epigastric pain for greater than three months.” Idiopathic gastroparesis is even more common than diabetic gastroparesis. Gastroparesis also more commonly occurs in women than men by three-fold. This holds true for all types of gastroparesis. Idiopathic gastroparesis is most commonly diagnosed in young or middle-aged women.7

Injury to the nerves or stomach muscles as a result of a virus is a potential cause for idiopathic gastroparesis. This diagnosis has been suggested in people who were previously healthy and then had an acute onset of illness caused by a virus, resulting in symptoms that persisted for more than three months with delayed gastric emptying. Some virus culprits suspected of causing gastroparesis include cytomegalovirus, Epstein-Barr virus, and herpes varicella-zoster. Symptoms in these individuals tended to be less severe with a good prognosis and symptoms slowly resolving in many.7

A cross-sectional prospective case control study (n=30) looked at immune profiling from endoscopic biopsies of those with idiopathic gastroparesis. The authors of the study sought to determine if there was a difference in immune cells and gene expression in the stomach and duodenal bulb. Increases in innate and adaptive immune cells were found in gastroparesis. There were also positive correlations between immune cell types with duration of disease, proton pump inhibitor dosing, and delayed gastric emptying.8 Although this research is in its infancy, it adds an additional potential layer to how gastroparesis is identified and treated.

Postsurgical Gastroparesis
Postsurgical gastroparesis (PSG) has been seen in those who have undergone an upper abdominal surgery at a rate of 0.4% to 5%. PSG can also be a complication of pylorus-preserving pancreatoduodenectomy, which occurs in 20% to 50% of patients early in the postoperative period. PSG has been reported in 50% to 70% of patients who have undergone pancreatic cancer cryoablation. Frequency of PSG varies directly with both the type and number of gastric operations performed. A vagotomy could cause loss of gastric parasympathetic control through various mechanisms. The interstitial cells of Cajal also may reportedly play a role in the pathogenesis of PSG. Gastric phase III, which is also known as the third phase of digestion or intestinal phase, becomes compromised after a gastrectomy. Normal digestion during this stage occurs via the duodenum’s response to chyme. Without the presence of a duodenum, there is no gastric phase III, which could result in gastric stasis.9

PSG can occur after a vagotomy for peptic ulcer surgery. Nissen fundoplications (in which the fundus part of the stomach becomes wrapped around the lower esophagus to tighten the lower esophageal sphincter) used to treat gastroesophageal reflux disease (GERD) and bariatric surgery for severe obesity have been linked to an increase in PSG. PSG has also been seen in patients after heart and lung transplants, which could be due to opportunistic viral infections or the result of immunosuppressive drugs, which can have motor-inhibitory effects. Many symptoms reported after abdominal surgery do resolve over time. This may occur due to an adaptation of the enteric nervous system to not having vagal “input” or reinnervation.10

There are two surgical interventions performed for gastric cancer: laparoscopic gastrectomy and open radical gastrectomy. Two risk factors for PSG in both surgeries are preoperative outflow tract obstruction and Billroth II anastomosis.11 Billroth II anastomosis involves removal of the stomach antrum with creation of an anastomosis of the remaining stomach to the side of the jejunum.12 Researchers found that patients who were more than 70 years old were also at risk for PSG if they had undergone an open radical gastrectomy. However, there was no increased incidence of PSG between either of the two surgical interventions.11

One study looked at the antroduodenal manometry recordings (records pressure waves produced in the stomach and small intestine) of 167 patients with gastroparesis between 2009 and 2019. Measurements were evaluated for fed period duration, number of phase III contractions (high amplitude contractions of the stomach and small intestine during hunger), migrating motor complexes (pattern of electromechanical activity in GI smooth muscle between meals), motility index (average of contractions in a time window of two minutes), and presence of neuropathic patterns. The fed period was significantly longer in those with idiopathic and diabetic gastroparesis vs those with postsurgical (p<0.05). The number and duration of phase III contractions and migrating motor complexes were significantly lower in idiopathic and diabetic gastroparesis compared with postsurgical (P<0.01); additionally, absence of migrating motor complexes during six-hour recording was observed more in idiopathic and diabetic gastroparesis (P<0.01 and p<0.05).13

Diagnosing Gastroparesis
There are several symptoms that can indicate a diagnosis of gastroparesis. These include heartburn or reflux (GERD), nausea, vomiting of undigested food, feeling full earlier than normal, stomach bloating or pain, and reduced appetite. Weight loss can occur due to taking in fewer calories than needed to meet one’s needs and/or because of eating less than prior to experiencing these symptoms. Symptoms range from mild to severe and can be exacerbated by solid foods, fatty foods, high-fiber foods, and/or carbonated drinks.3 Fatty foods and high-fiber foods already naturally take longer to digest, thus exacerbating symptoms in those with gastroparesis. Carbonated drinks can create a feeling of fullness, adding to the symptom of feeling full too early or exacerbating symptoms of GERD. Symptoms can greatly impair a person’s quality of life and lead to disability in 1 out of 10 patients with gastroparesis. Gastroparesis symptoms typically follow a pattern of cycles with flare-ups, sometimes persisting for years.14

Gastric Emptying Studies
There are several ways to diagnose gastroparesis. One way is a gastric emptying study. According to the Mayo Clinic, this is the most important test to use when diagnosing gastroparesis. A patient undergoing this test eats a light meal, such as eggs or toast, which contains a small amount of radioactive material. A scanner that can detect the movement of this material is put over the patient’s abdomen and the rate at which food leaves the stomach is monitored, tracking how long it takes for the stomach to empty the meal. The test typically takes four hours to complete, and it’s recommended that patients stop taking any medications that could potentially slow gastric emptying prior to the test.15,16

Two less common gastric emptying studies include a breath test and a wireless motility study. For a gastric emptying breath test, the patient eats a meal containing a substance that’s absorbed in the intestines and passes into the breath. Samples of the breath are collected over four hours.16

In a wireless motility study, the patient swallows a small electronic motility capsule, known as a SmartPill. The capsule moves through the entire digestive tract and sends information, such as the rate of stomach emptying and how quickly liquid and food move through the large and small intestine, to a recorder that’s either hung around the patient’s neck or clipped to a belt. This capsule naturally passes through the body via a bowel movement.16

Upper GI Endoscopy and Ultrasound
An upper gastrointestinal endoscopy is another test performed to diagnose gastroparesis. A tiny camera on the end of a long, flexible tube is used to examine the upper digestive system—including the esophagus, stomach, and duodenum of the small intestine—to determine whether any abnormalities exist. An ultrasound, wherein high-frequency sound waves are used to produce images of particular structures within the body, is another test method. For diagnosing gastroparesis, ultrasound images areas of the GI tract that may show abnormalities.15

Upper GI Series
Another test used to diagnose gastroparesis is an upper GI series, which is performed with a series of X-rays. The patient drinks a white, chalky barium liquid, which coats the digestive system, highlighting any abnormalities.15 Both the upper GI series and ultrasound tests can show intestinal obstructions that may indicate gastroparesis.16

Complications
Several complications can occur because of gastroparesis, including GI obstruction, small intestinal bacterial overgrowth (SIBO), inconsistent blood sugar levels, and malnutrition.

Obstruction
In more severe cases of gastroparesis, food residue left in the stomach can congeal to form an obstruction in the GI tract called a bezoar. This is a solid mass formed from undigested fibers. These fibers can include cellulose, hemicellulose, lignin, and fruit tannins. People with gastroparesis may need to avoid foods that contain these fibers to help prevent the formation of a bezoar. Certain medications, such as cholestyramine, sucralfate, enteric-coated aspirin, aluminum-containing antacids, and bulk-forming laxatives can also cause bezoars.15 Increased nausea and vomiting may be a sign of the presence of a bezoar, which should be examined via endoscopy.15 Treatment may include enzyme therapy, lavage, or endoscopic therapy to break up the bezoar using mechanical methods.15

Bacterial Overgrowth
Gastroparesis patients, especially those who also have diabetes or have undergone a vagotomy, are at an increased risk of developing SIBO, often marked by abdominal pain and bloating. One study of 50 participants with gastroparesis used a glucose breath test to detect the presence of SIBO. Of those participants, 60% had a positive breath test; SIBO was most common in those who had experienced symptoms of gastroparesis for a longer period.17

Diet may need to be altered in those with SIBO. Some may not be able to tolerate lactose or certain carbohydrates well. Treatment typically includes the use of antibiotics. Rifaximin has been found to have positive effects in improving symptoms and eliminating bacterial overgrowth in up to 80% of those who were treated with it. Treatment is typically a seven- to 10-day course and higher doses (1,200 or 1,600 mg daily) were found to be more effective than standard doses (600 or 800 mg daily).18 A meta-analysis compared probiotic usage for treatment of SIBO to those without probiotic usage. Those who used probiotics for treatment had a significantly higher “decontamination rate” than those in the nonprobiotic group.19

Worsened Diabetes
While diabetes can be linked to gastroparesis, particularly due to vagus nerve damage, gastroparesis itself can cause difficulties with blood sugar management, including sudden drops and wide variations in blood sugar in those who are insulin dependent.20 In those with diabetes who haven’t been diagnosed with gastroparesis, variable blood sugar measurements may indicate gastroparesis.

From a blood sugar standpoint, gastroparesis could be likened to skipping a meal. It takes much longer for digestion to occur and thus for glucose to be taken up into cells. The pyloric valve controls stomach emptying, which could occur partially within minutes and completely within three hours under normal circumstances. However, if the valve is closed tight, then the full stomach emptying could take several days. In this case, although the patient has eaten a meal, their blood sugar could drop within one to two hours after eating and rise suddenly several hours later. Thus, hypoglycemia is a major concern for people with diabetes who are insulin dependent, and the factor of unpredictability makes blood sugar management difficult.20

Fortunately for those who aren’t insulin dependent (typically patients with type 2 diabetes), hypoglycemia is less of a concern and blood sugars are not typically as erratic. Only basal insulin will be released if the stomach doesn’t empty. However, sulfonylurea medications and some orally administered hyperglycemic agents can still cause hypoglycemia, and the use of these medications should be considered for people with diabetes who also have gastroparesis.20

Malnutrition
Malnutrition can occur in those with gastroparesis, typically due to lack of appetite and early satiety. This puts patients at risk of weight loss and poor oral intake. Nausea and vomiting, other gastroparesis symptoms, also can impair nutrient absorption. Comparing a patient’s usual body weight with their current weight may be one indicator of malnutrition. A nutrition-focused physical exam confirms other signs, such as fat or muscle loss. Exact guidelines for determining malnutrition will vary by facility, but the American Society for Parenteral and Enteral Nutrition provides universal guidelines. Those at risk are typically identified using the following criteria: They’re at less than 80% of their ideal body weight, have a BMI lower than 20, have lost 5% of their usual body weight in one month, or have lost 10% of their usual body weight in six months.21

Treating Gastroparesis
Health care professionals can have a significant impact on gastroparesis treatment through diet education and lifestyle recommendations. Medications and dietary changes are often first-line treatments. If necessary, additional interventions, such as gastric pacemakers, gastric electrical stimulation, or a venting gastrostomy, are used. Nutrition support may also be necessary.

Diet
Proper nutrition can not only alleviate symptoms of gastroparesis but also help prevent malnutrition and dehydration. Typical MNT recommendations include following a low-fat, low-fiber diet; eating five to six small meals daily instead of two or three larger meals; and consuming softer, well-cooked foods or puréed/liquid foods.12 Additional recommendations include chewing foods well, avoiding carbonated beverages and alcohol, hydrating well, and consuming sports drinks or oral rehydration solutions as needed. Low-intensity exercise, such as walking, can be helpful after consuming a meal, and patients should avoid lying down for two hours after eating a meal. Depending on the patient’s medical history and present status, vitamin/mineral supplementation may be necessary.22

Medications
Several medications are used to treat gastroparesis, typically prokinetic or promotility agents, which can help the stomach empty more quickly. Another common drug for gastroparesis that’s been FDA approved since 1983, metoclopramide, has shown improvement in about 40% of patients in clinical trials. However, a potential side effect of taking metoclopramide is the serious movement disorder tardive dyskinesia, so it’s not typically recommended to be taken for more than 12 weeks.23

Erythromycin is another common drug used to treat gastroparesis. This is an antibiotic similar in structure to motilin, which is a hormone that shortens stomach emptying time. Many people with diabetes are deficient in motilin, and researchers have determined that 40% of patients show an improvement in symptoms with only short durations of taking erythromycin. Domperidone is a drug used to increase muscle contractions within the stomach wall, but it’s only available through a particular FDA program and typically not used in the United States.23

A randomized placebo-controlled trial (n=152) demonstrated promising results for the use of tradipitant, a drug currently under clinical trials, in patients with diabetic and idiopathic gastroparesis. Patients receiving tradipitant had a significant decrease in nausea at week four compared with placebo (p=.0099) and significant increase in nausea-free days (p=.0160). This was even greater for those with nausea and vomiting at baseline.24

While antiemetic agents are used to treat nausea and vomiting associated with gastroparesis, they don’t treat gastroparesis itself. Initial, small research studies show a potential for botulinum toxin injections as a treatment, but overall results are mixed, and it’s not typically recommended at this time.23

Gastric Pacemaker
Another treatment for gastroparesis is laparoscopic surgical placement of a gastric pacemaker. The gastric pacemaker includes a neuroregulator to send signals to the vagus nerve to help regulate digestion, a lead system that controls the electrical pulses sent to the vagus nerve, and an external control system to allow the patient to adjust settings.25

One study demonstrated success of this procedure in its treatment of gastroparesis. A group of 25 patients with gastroparesis (19 with diabetic gastroparesis, three with postsurgical gastroparesis, and three with idiopathic gastroparesis) had gastric pacemaker implantation between April 1998 and September 2000. All of these participants demonstrated delayed gastric emptying via radionucleotide study. Results showed that both severity and frequency of nausea and vomiting improved significantly at both three and 12 months, and gastric emptying time shortened.26

Gastric Electrical Stimulation
Another form of treatment for gastroparesis is gastric electrical stimulation (GES). Low-energy electrical stimuli are transmitted into the muscularis propria portion of the stomach, with a frequency above the normal activity of three cycles per minute seen in gastric slow waves. This treatment differs from gastric pacing due to the frequency delivered. A meta-analysis performed by the National Institutes of Health shows the potential this type of treatment holds for those with refractory gastroparesis. Significant decreases in nausea and vomiting, need for enteral and parenteral nutrition support, and improvement in gastric emptying were seen.27

The benefits of this treatment option can also be seen in patients with both diabetes and gastroparesis. One study looked at a retrospective review of 48 adult patients with diabetes who underwent GES. There was significant improvement in upper GI symptoms (eg, vomiting, early satiety, bloating, and postprandial fullness), health-related quality of life, nutritional status, glucose control, and hospitalizations at both six and 12 months, with low complication rates.28

Gastric Peroral Endoscopic Myotomy
Gastric peroral endoscopic myotomy (G-POEM) is a new procedure developed by Mouen Khashab, MD, at John Hopkins Medicine. G-POEM involves an endoscope being inserted through the mouth to cut the muscles near the pyloric sphincter, to help relax the sphincter and allow food to empty freely.29 A study found significant improvement in symptoms and gastric emptying at six months postprocedure in patients who had undergone G-POEM vs sham procedure (p=0.005).30

Venting Gastrostomy
A venting gastrostomy may also be used to help relieve symptoms of gastroparesis. An opening is created in the abdominal wall and a tube is placed into the stomach. Stomach contents can then flow out to relieve pressure in the stomach.22 Venting gastrostomies are typically used for those experiencing nausea, vomiting, and bloating. Gastrostomy-jejunostomy tubes may be used to provide gastric decompression and enteral feedings simultaneously.31 Fluid and electrolyte balance will require close monitoring and additional IV fluids will likely be needed.

Nutrition Support
If the gastroparesis symptoms are severe and/or a significant weight loss has occurred, nutrition support may be warranted. Oral or nasal feeding tubes may be placed into the small intestine. If the tube feeding is needed long term, then a jejunostomy tube is typically placed for feeding. This tube goes into the jejunum, a part of the small intestine, therefore bypassing the stomach. Another option is a percutaneous endoscopic transgastric jejunostomy, which enables both decompression and feedings.21

Patients with a jejunostomy tube cannot tolerate bolus feeds, but most can consume a standard, polymeric formula. If a gastric tube is used/tolerated, then a more calorically dense formula may be necessary. For those who have problems with bacterial overgrowth, a no-fiber formula is recommended. If tube feedings are not tolerated, then parenteral nutrition may be needed as a last resort. In that case, clinical status and labs should be monitored closely.21 Some will experience refractory gastroparesis and be able to return to eating orally.16

Nutrients of Concern
Patients with gastroparesis are at risk of malabsorption of several nutrients. Iron-deficiency anemia is of particular concern, usually due to red meat intolerance, reduced gastric acid production from the use of proton pump inhibitors, or a vagotomy. Iron supplementation may be necessary, and the oral route is preferred. Recommendations are to supplement with 200 mg of elemental iron daily. Iron replacement therapy is usually given three times per day and each dose is recommended to be given six hours apart. Vitamin C may enhance iron absorption and the addition of 25 to 50 mg is recommended with each iron supplement as well.21

There may be a vitamin B12 deficiency following a gastrectomy due to reduced levels of gastric acid and/or intrinsic factor. Bacterial overgrowth and a reduction in vitamin B12-rich foods may also be contributing factors. Supplementation dosing depends on severity of deficiency. Supplementation recommendations for mild deficiencies is 500 to 1,000 mcg/day. Severe deficiencies may require intramuscular or subcutaneous injections of 100 to 200 mcg monthly. Of note, the percentage retained from larger doses of vitamin B12 is less than in lower doses.21

Vitamin D is also of concern for patients who have undergone gastrectomies, usually due to reduced lactose intake and/or poor absorption and metabolism of vitamin D. This can result in accelerated bone loss and lead to osteoporosis. There are guidelines for supplementation of vitamin D and calcium. Recommendations for patients with bone disease are 1,500 mg of calcium and 800 IU of vitamin D daily. Maximal absorption occurs when calcium is provided in doses of 500 mg or less.21 Calcium citrate is more easily absorbed and is also preferred for those who take histamine-2 blockers or protein-pump inhibitors.32 One meta-analysis found that vitamin D3 was more effective at increasing serum 25(OH)D concentrations in comparison with vitamin D2.33

Putting It Into Practice
When assessing patients or clients with gastroparesis, there are several things to bear in mind. Weight loss is a common occurrence, so current body weight at each follow-up should be compared with baseline body weight. Weight status along with oral intake and or signs of fat/muscle wasting could determine a possible malnutrition diagnosis.

Dietitians play a crucial role in the lives of those with gastroparesis. Providing recommendations for a low-fat, low-fiber diet and five to six small meals per day is standard for many patients. However, each patient’s plan of care will be individualized. Most patients will have no delay in emptying liquids, despite a delay in emptying solids. Patients typically have increased difficulty with solids as the day goes on and do better with liquids later in the day. They also may be able to better tolerate puréed foods at this time because, once puréed foods are mixed with saliva and gastric secretions, they become liquefied.21

Clinicians can educate and work with patients and clients to individualize their needs and improve their caloric and nutrient intake, which can help alleviate symptoms and improve quality of life. If nutrition support is warranted, recommending the appropriate route of feeding and formula for the patient is critical. Individuals able to tolerate enteral nutrition typically are fed via jejunostomy tube. The goal is always to prevent unplanned weight loss and malnutrition. In addition, working with the gastroenterology team is important for providing the best plan of care for the patient. If the patient does not currently visit a gastroenterology specialist, recommending or referring them to one should be part of the care plan.

There are a number of ways care providers can collaborate in treating patients with gastroparesis. RDs will be able to best assess which nutrients may require supplementation and are the experts in providing recommendations for enteral and parenteral nutrition. RDs may also assist in helping patients achieve or maintain an appropriate weight.

Any client who shows significant symptoms of gastroparesis, experiences significant weight changes, is unable to tolerate a diet by mouth, or has had a significant functional change occur would be a candidate for consultation; the involvement of a gastroenterologist will benefit patients as well.

— Lauren Botelho, MS, RD, LDN, is a dietitian in the Boston area. Botelho has worked in inpatient settings, outpatient settings, and long-term care. She has a BFA in writing, literature, and publishing, and is a freelance nutrition writer. Additionally, Botelho is a family nurse practitioner who works in gastroenterology.

Learning Objectives
After completing this continuing education course, nutrition professionals should be better able to:
1. Explain the different types of gastroparesis and how they are identified.
2. Identify malnutrition in those with gastroparesis and nutrition-related issues affecting patients with gastroparesis.
3. Counsel clients on the different treatment options for gastroparesis and how to apply the role of nutrition support.
4. Identify how to assess clients with gastroparesis using MNT.

Examination
1. What are two main causes of gastroparesis?
a. Muscle damage and poor nutrition
b. Nerve damage and muscle damage
c. Nerve damage and decreased gastric acid
d. Poor nutrition and decreased gastric acid

2. What are the three main types of gastroparesis?
a. Diabetic, idiopathic, postsurgical
b. Idiopathic, postsurgical, renal
c. Diabetic, renal, idiopathic
d. Diabetic, postsurgical, nutrient deficient

3. Which percentage of those affected by gastroparesis are women?
a. 5%
b. 80%
c. 25%
d. 50%

4. Which nutrients can exacerbate gastroparesis symptoms?
a. High fat, low fiber
b. High fiber, low fat
c. High fat, high fiber
d. Low fat, low fiber

5. What is a major concern for type 1 diabetics with gastroparesis?
a. Elevated A1c
b. Hypoglycemia
c. Decreased appetite
d. Weight gain

6. What are two potential indicators of malnutrition in patients with gastroparesis?
a. A 5% weight loss in one month and poor oral intake
b. A 10% weight loss in one year and poor oral intake
c. A 5% weight gain in one month and nausea
d. A 10% weight gain in one year and vomiting

7. What type of medication is typically recommended for patients with gastroparesis?
a. Calcium channel blockers
b. Statins
c. Sulfonylureas
d. Prokinetic agents

8. What nutrients are at risk of deficiency in patients who have undergone vagotomies and gastrectomies?
a. Thiamine, niacin, folic acid
b. Iron, vitamin D, vitamin B12
c. Vitamin D, thiamine, niacin
d. Folic acid, thiamine, vitamin B12

9. Most patients with gastroparesis will have preserved function of which of the following?
a. Emptying of solids
b. Emptying of supplements
c. Emptying of liquids
d. Emptying of high-fat foods

10. What are two complications from gastroparesis?
a. Malnutrition and obstruction
b. Obstruction and weight gain
c. Bacterial overgrowth and weight gain
d. Worsened diabetes and increased appetite

References
1. Gastroparesis. John Hopkins Medicine website. https://www.hopkinsmedicine.org/health/conditions-and-diseases/gastroparesis#:~:text=Gastroparesis. Updated 2023. Accessed September 16, 2023.

2. What is gastroparesis? GastroparesisClinic.org website. https://www.gastroparesis.mindovergut.com/what-is-gastroparesis/. Updated February 1, 2021. Accessed September 16, 2023.

3. Smith L. Gastroparesis: what you need to know. Medical News Today website. https://www.medicalnewstoday.com/articles/313873. Updated June 20, 2023. Accessed September 16, 2023.

4. Mandal A. Gastroparesis epidemiology. News Medical Life Sciences website. https://www.news-medical.net/health/Gastroparesis-Epidemiology.aspx. Updated January 23, 2023. September 16, 2023.

5. Parkman HP, Fass R, Foxx-Orenstein AE. Treatment of patients with diabetic gastroparesis. Gastroenterol Hepatol (N Y). 2010;6(6 Suppl 9):1-13.

6. Diabetic neuropathy. National Institute of Diabetes and Digestive and Kidney Diseases website. https://www.niddk.nih.gov/health-information/diabetes/overview/preventing-problems/nerve-damage-diabetic-neuropathies/all-content. Updated February 2018. Accessed September 16, 2023.

7. Parkman HP. Idiopathic gastroparesis. Gastroenterol Clin North Am. 2015;44(1):59-68.

8. Gottfried-Blackmore A, Namkoong H, Adler E, et al. Gastric mucosal immune profiling and dysregulation in idiopathic gastroparesis. Clin Transl Gastroenterol. 2021;12(5):e00349.

9. Dong K, Yu XJ, Li B, Wen EG, Xiong W, Guan QL. Advances in mechanisms of postsurgical gastroparesis syndrome and its diagnosis and treatment. Chin J Dig Dis. 2006;7(2):76-82.

10. Shafi MA, Pasricha PJ. Post-surgical and obstructive gastroparesis. Curr Gastroenterol Rep. 2007;9(4):280-285.

11. Meng H, Zhou D, Jian X, Ding W, Lu L. Incidence and risk factors for postsurgical gastroparesis syndrome after laparoscopic and open radical gastrectomy. World J Surg Oncol. 2013;11:144.

12. Cresci G, Escuro A. Medical Nutrition Therapy for Upper Gastrointestinal Disorders. In: Mahan LK, Raymond JL, eds. Krause’s Food & The Nutrition Care Process. 14th ed. St. Louis, MO: Elsevier; 2017:520-523.

13. Hereijgers MJM, Keszthelyi D, Kruimel JW, Masclee AAM, Conchillo JM. Antroduodenal motility recording identifies characteristic patterns in gastroparesis related to underlying etiology. Neurogastroenterol Motil. 2022;34(11):e14394.

14. Gastroparesis. National Organization for Rare Disorders website. https://rarediseases.org/rare-diseases/gastroparesis/. Updated March 16, 2012. Accessed September 16, 2023.

15. Gastroparesis. Mayo Clinic website. https://www.mayoclinic.org/diseases-conditions/gastroparesis/diagnosis-treatment/drc-20355792. Updated March 30, 2019. Accessed August 27, 2019.

16. Diagnosis of gastroparesis. National Institute of Diabetes and Digestive and Kidney Diseases website. https://www.niddk.nih.gov/health-information/digestive-diseases/gastroparesis/diagnosis. Updated January 2018. Accessed April 10, 2019.

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