The digestive roles of the stomach
The efficacy of nutrition therapy for gastroparesis is rooted in an understanding of the two predominant functions of the stomach: (1) it serves as a reservoir for ingested food, and (2) it grinds, mixes, and triturates that food into particles small enough to enter the small intestine. To accommodate ingested food, the fundus relaxes and expands from 50 mL to up to 4 L. This is followed by recurrent three-minute peristaltic waves that mill food into 0.5- to 2-mm particles. Each peristaltic wave also empties 2–4 mL of chyme through the pylorus and into the duodenum, which translates into a nutrient emptying rate of 1–4 kcal/min (60–240 kcal/hr). Between meals, the migrating motor complex produces slow peristaltic waves that clear chyme and debris out of the stomach into the duodenum and move it along distally through the intestines.
Gastroparesis can be a manifestation of a breakdown in any component of gastric function, including the inability of the fundus to accommodate food volumes, abnormal interstitial cells of Cajal (ICC; also known as pacemaker cells), insufficient smooth muscle contraction or enteric neuron activity, and/or pylorus dysfunction. Any of these disruptions can result in poor milling and slower emptying.
Symptoms of gastroparesis and nutrition implications
Common symptoms of gastroparesis tend to impact a patient’s diet, weight, and overall nutrition status. At the same time, symptoms can also be generated or exacerbated depending on a patient’s diet. They include:
Poor glycemic control in patients with DM
Symptoms vary in type and severity among patients may depend on the underlying etiology. They may also wax and wane over time in the same patient. If not addressed, these symptoms can result in:
Vitamin and mineral deficiencies
Unintentional weight loss or gain
Loss of lean muscle mass
Inability to enjoy the social aspects of eating
Compromised overall quality of life
Disrupted eating habits and less healthy dietary choices
Nutrition therapy for gastroparesis
Having a heterogeneous pathogenesis requires a heterogeneous approach to treatment for gastroparesis, involving both nutrition and medical management. Nutrition is an essential consideration, as the volume, texture, frequency, and specific composition of foods can affect how quickly they empty from the stomach. Nutrition therapy is aimed at mitigating symptoms and reducing the incidence of flares, while also correcting nutrient deficits and ensuring long-term nutrition and hydration needs.
Given the heterogeneity and fluctuation of symptoms, an individualized approach is best. Moreover, patients with gastroparesis exhibit a wide variety of food intolerances that may ebb and flow over time. Some patients achieve adequate relief with minor dietary adjustments, while others have persistent difficulties that ultimately require enteral or parenteral nutrition. Even after specific dietary modifications have been successfully implemented, clinicians and patients should continue to try new foods and approaches as tolerated.
Nutrition therapy begins with a comprehensive nutrition assessment to determine the patient’s baseline nutritional status and identify the appropriate dietary modifications. Screening for malnutrition in this patient population is vital, as persistent symptoms can lead to inadequate nutrition, which in turn can worsen symptoms further . The Academy of Nutrition and Dietetics and the American Society for Parenteral and Enteral Nutrition have established screening guidelines for both the inpatient and outpatient setting. According to these guidelines, a diagnosis of malnutrition is warranted in the presence of two or more of the following criteria :
Insufficient energy intake
Unintended weight loss
Loss of subcutaneous fat
Loss of muscle mass
Reduced hand grip strength
Unintentional weight loss is one of the most telling indicators of nutrition status. However, be advised that weight can often be confounded by fluid status, especially in the setting of vomiting and/or dialysis. Likewise, patients with stable weight or high body mass index may still have accrued nutrient deficits by way of a poor-quality diet low in protein, essential fatty acids, vitamins, and minerals. The downstream effects of malnutrition are momentous and include: muscle loss/weakness, reduced functional capacity, increased risk of poor healing of pressure ulcers (especially in the diabetic patient with poor circulation and/or hypoalbuminemia with secondary third spacing), poor glycemic control, and prolonged and recurrent hospital admissions .
Nutrient intake in individuals with gastroparesis is known to be sub-optimal. In a survey of 305 GP patients, 64% were found to have an energy-deficient diet, meeting less than 60% of their daily nutrition needs . A previous study found that patients with gastroparesis consumed significantly fewer calories than healthy controls (1112 kcal vs 1431 kcal), along with significantly less vitamin B12, vitamin C, folate, thiamine, niacin, magnesium, phosphorus and zinc; intake of vitamin B6, riboflavin, thiamine, calcium, copper, and iron were also below the recommended dietary allowance . Furthermore, vomiting can subsequently result in excessive mineral and nutrient losses.
To determine the most appropriate diet modifications, a diet history should include typical foods eaten, size and frequency of meals, and types of foods tolerated and not tolerated. A nutrition assessment should also include the frequency, pattern, and description of symptoms, nutrition interventions previously tried, current medications and supplements, dentition, and bowel habits. Finally, in patients who present with chronically inadequate and/or poor-quality PO intake, consider obtaining baseline nutrition labs (especially 25(OH) Vitamin D, serum B12, methylmalonic acid, ferritin, RBC folate, and HgA1c in DM patients). Of note, albumin and prealbumin are not accurate reflections of nutrition status, albeit still very frequently used in the general hospital setting as a means of determining nutritional and/or protein status. While they are indicative of an inflammatory state and/or severity of illness, they should not be used to identify or rule out malnutrition. See Box 23.1 for information to gather and include during a nutrition assessment.
|Include the following in your assessment of a patient with gastroparesis:|
The current body of research on dietary modifications for gastroparesis has consisted mostly of small trials or observational studies that are far from conclusive. Most of the diet suggestions that follow are based on what is physiologically rational and supported by clinical experience, rather than the limited data currently available. Advise patients that they may need to undergo some trial and error before finding what works best for them. Likewise, remind them that their symptoms and tolerances to individual foods can ebb and flow. Foods should only be avoided or limited if they are known to induce symptoms, and routine experimenting should be encouraged to ensure that patients are not overly or unnecessarily restricting. While prioritizing nutritious foods over empty calories is a good rule to follow, keep in mind that in severely malnourished patients and/or patients approaching the need for nutrition support, any calorie is a good calorie, and prior diet restrictions may need to be lifted so that basic nutrition needs can be met.
Consistency: Liquids, purees, and solids
Many gastroparetic patients report better tolerance of liquids and purees versus solids. Olausson et al demonstrated that a “small particle diet” improved nausea/vomiting, fullness, bloating, lower abdominal pain, regurgitation, and heartburn (all symptoms measured with the exception of upper abdominal pain) compared to a control diet of large particle sizes. Some patients may tolerate solid foods in the morning but may need to transition to liquids or purees as the day progresses. In the event of severe symptoms or flare ups, they may need to follow a strictly liquid or pureed diet. Box 23.2 contains specific suggestions for liquid and pureed food. Bear in mind that many of the commercially available meal replacement shakes are high in sugar, which may be problematic for patients who need to reduce their sugar intake in the setting of small intestinal bacterial overgrowth. Patients with diabetes should be educated on the importance of overall consistency of carbohydrate intake at each meal or snack rather than the source of those carbohydrates in controlling blood sugar. Many liquid and pureed foods are best fortified with protein powders and calories from lipids/fats to maximize calorie intake per meal and better help meet daily caloric needs.
Note that bypassing the act of chewing carries the risk of consuming these foods too quickly. Even with liquids and purees, patients may need to be reminded to pace themselves to allow for proper gastric emptying and avoid the sensation of fullness and abdominal discomfort.
Volume: Small, frequent meals
Large meals have been shown to slow gastric emptying . Patients with gastroparesis may benefit from eating smaller volumes at a time with more frequency (5–6 times) throughout the day. While small, frequent meals may be helpful, patients should be instructed to avoid constant grazing, which can disturb the migrating motor complex and inhibit total gastric emptying. Rather, meals should still have a defined beginning and end with some amount of time in between. A patient’s gastric emptying study can provide a guideline for transit time and how frequently he/she can eat.
If smaller meals are needed, instruct patients on how best to meet their calorie and protein needs, either by eating more frequently, choosing high-calorie, high-protein foods for each meal, keeping to a liquid diet, or alternating between liquids and solids. Discuss ways to make everything that enters the GI tract count, such as taking medications with calorie- and protein-containing beverages and adding condiments to meals. See Box 23.3 for more suggestions on ensuring adequate intake.
Some research suggests that a low-fat diet may prevent symptom exacerbation in gastroparesis, but studies thus far have been small and problematic. From a physiological perspective, dietary fat activates cholecystokinin (CCK), resulting in fundic relaxation, inhibition of antral motility, and delayed gastric emptying. In a recent small study of 12 patients with idiopathic or DM gastroparesis, Homko et al. demonstrated that overall symptom control is best achieved with a diet consisting of only low-fat liquids, followed by low-fat solids, then high-fat liquids, and finally high-fat solids . However, liquid fats have been shown to be well tolerated in gastroparesis patients. Unless a fat-containing food or liquid clearly causes or worsens symptoms, it should not be limited, especially in patients who are underweight and/or malnourished; liquid fats, such as plant-based oils and dairy products, provide a great source of calories for much less volume compared to carbohydrates and protein.
A diet high in fiber can reduce antral motility and delay gastric emptying in many individuals regardless of the presence of gastroparesis, potentially inducing premature satiety and preventing adequate intake of other essential nutrients . In patients with gastroparesis, fiber may also exacerbate abdominal distension, gas, bloating, and reflux.
Some patients with gastroparesis, particularly those with severe dysmotility, are at risk for developing bezoars. A bezoar is a mass of fiber that remains undigested and collects in the stomach. It must often be either broken up with enzymes, cola therapy with nasogastric lavage, or endoscopic fragmentation and moved along with prokinetics, although sometimes surgical extraction is necessary . High-risk patients should be instructed to avoid fibrous and high-fiber foods, such as apples, potato peels, shredded coconut, Brussels sprouts, beans, nuts, and seeds (see Table 23.1 for additional foods).