Running head: NUTRITIONAL APPROACHES TO GASTROPARESIS 1

NUTRITIONAL APPROACHES TO GASTROPARESIS

SNEHA LAKHOTIA
Marywood University
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NUTRITIONAL APPROACHES TO GASTROPARESIS

Introduction

Gastroparesis is a syndrome of delayed gastric emptying in the absence of a mechanical

obstruction characterized by nausea, vomiting, early satiety, and abdominal discomfort

(Camilleri, Parkman, Shafi, Abell, & Gerson, 2013). The number of individuals affected by

symptoms of gastroparesis in the United States is estimated to be over 4 million (Stein, Everhart,

& Lacy, 2015). Although, high prevalence of gastroparesis has been reported in type 1 diabetics

(40 %) and type 2 diabetics (10–20 %), these studies were from tertiary academic medical

centers where the prevalence is expected to be higher than the general population; the

community prevalence was estimated to be ∼ 5 % among type 1 diabetics, 1 % among type 2

diabetics, and 0.2 % of controls in Olmsted County, Minnesota (Choung et al., 2012).

Gastroparesis usually arise from autonomic nerve injury related to diabetes, surgery, or

antecedent infections, though the largest disease subcategory remains idiopathic (Parkman,

2015). Apart from the need for blood glucose optimization in patients with diabetes, nutritional

recommendations in gastroparesis tend not to be etiologically specific. Although, some

practitioners regard these recommendations as broadly relevant but specific data is lacking

regarding optimal nutritional strategies within this population. Complications of gastroparesis

not only lead to increased morbidity and mortality, increased hospital stay, and significant

nutritional deficits, but also impact the overall quality of life of those affected. While several

options exist for pharmacologic and mechanical intervention among patients with gastroparesis,

this review will focus on the existing evidence based nutritional approaches to gastroparesis.
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Dietary Management

The American College of Gastroenterology (ACG) guidelines advocate dietary

modifications as the first line therapy for gastroparesis management. The choice of nutritional

support depends on the severity of the disease. In mild gastroparesis, oral nutrition is the goal

therapy whereas in severe cases enteral or parenteral nutrition support may be needed (Camilleri

et al., 2013).

Oral Nutrition

Traditional dietary recommendations to minimize the symptoms and maximize tolerance

of oral intake include small, frequent meals 4-5 times a day or more to maintain adequate daily

caloric intake. Restriction of dietary fat (e.g. fried foods, fatty meats, creamy sauces, peanut

butter) is indicated as fat slows gastric emptying. Foods such as lean meats or eggs, nutritional

supplements, milk shakes are well tolerated and should be included. Dietary fiber is restricted

and dietitian should advise soluble fiber. Avoid seeds, nuts, whole wheat products, non-

digestible fiber (e.g. fresh fruits and vegetables) as they require effective interdigestive antral

motility that is frequently absent in patients with significantly delayed gastric

emptying. Emphasis is made on consumption of liquids for patients who are unable to tolerate

solid foods. Foods such as evaporated milk, protein powder, ice cream, strained purees of solid

foods can add calories to the diet (Camilleri et al., 2013; Parrish, 2015).Carbonated beverages

can aggravate gastric distension and should be restricted in the diet (Camilleri et al., 2013).

Alcohol and smoking should also be avoided as they can decrease antral contractility and delay

gastric emptying (Bujanda, 2000; Miller, Palmer, Smith, Ferrington, & Merrick, 1989).
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In a nut shell, foods that are acidic, spicy, roughage based, fatty increase the symptoms of

gastroparesis and thus should be avoided (Wytiaz, Homko, Duffy, Schey, & Parkman, 2015;

Homko, Duffy, Friedenberg, Boden, & Parkman, 2015). Depending on the severity of the disease

and patient tolerance to the diet it is gradually advanced from thin liquids, pureed foods and

latter to solid foods (Stuart P.S., 2017).

All of these approaches are largely based on clinical experience as trial based evidence to

support these interventions is lacking (Homko et al., 2015). A study was conducted on 12

participants with gastroparesis receiving one of the four meals on four separate days in a

randomized order (high- fat solid, high -fat liquid, low -fat solid and low-fat liquid meals). It was

found that high fat solid meal increased overall symptoms whereas 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 (Homko et al., 2015). A slightly larger study

was conducted by the same group where 45 participants with gastroparesis participated. Food

Toleration and Aversion Survey was administered asking patients about experiences eating

certain foods. Foods characterized as fatty, acidic, spicy and roughage-based aggravate

symptoms while bland, sweet, salty and starchy were tolerable (Wytiaz et al., 2015).

Emerging dietary considerations for oral nutrition in patients with diabetic gastroparesis

include a small particle size diet. A characteristic feature of this diet is that food should be easy

to mash with a fork into small particle size, e.g. mashed turnips. The diet excludes foods with

husks or peels, membranes, stringy foods, seeds and grains, compact poorly digestible particles

and white fresh bread. Foods such as corn, peas and almonds if they were mashed in a processor

with a similar consistency like mashed turnip or ground to a powder were included in the diet.
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Fifty-six participants were randomized into two groups i.e. control diet and the intervention diet

or small particle size diet. A significant greater reduction was found on the gastroparetic

symptoms such as nausea/ vomiting, postprandial fullness and bloating despite higher fat intake

in the intervention diet. Longer duration studies might change the recommendations (Olausson et

al., 2014). Some investigators have also stated role of low FODMAPS (fermentable oligo-, di-

and monosaccharides and polyols) diet among patients with gastroparesis but particularly in

context of irritable bowel syndrome (Eswaran, Chey, Han-Markey, Ball, & Jackson, 2016).

Complementary therapy may benefit patients with antiemetic properties. Ginger has not

been studied much in the context of gastroparesis but it has shown benefit in chemotherapy

induced nausea (Ryan et al., 2012). It has also reported to improve upper gastrointestinal

symptoms and accelerates gastric emptying and stimulates antral contractions in healthy

volunteers (Wu et al., 2008). Products of ginger such as ginger ale has also found to be tolerated

by patients with gastroparesis (Wytiaz et al., 2015).

Recurrent vomiting and poor oral intake make it difficult to maintain hydration and

nutritional status among patients with gastroparesis. Thus, resulting in increased risk for weight

loss, deficiency of vitamins and minerals and malnutrition. The NIDDK Gastroparesis Clinical

Research Consortium (GpCRC), (2011) conducted an observational study on 305 participants

with gastroparesis on oral intake. It demonstrated that 64% of them had calorie deficient diet and

the data suggest that particularly common micronutrient deficiencies include iron, folate,

thiamin, calcium, magnesium, potassium, zinc and vitamin B12, C, D, E and K. A recent study

demonstrates that increased calorie intake and reduced energy expenditure resulted in weight

gain among this population indicating overweight status can neither prevent diagnosis of

gastroparesis nor malnutrition (Homko, Zamora, Boden, & Parkman, 2014).

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Nutrition Support

For patients whose oral intake is inadequate, enteral route is the preferred method of

feeding rather than parenteral nutrition. This is mainly because of safety, lower cost and ease of

use. Prior to initiation of enteral feeds consider the following: patient’s wishes, unintentional,

progressive weight loss (e.g. greater than 5-10% over 3-6 months, or consistently below agreed

upon goals); frequent hospitalizations for dehydration or metabolic disarray; an inability to

reliably take oral medications; poor quality of life or failure to thrive. The vast majority of

patients will tolerate standard enteral formulations, though hospitalization is usually required for

initiation of feedings, particularly among patients with labile blood glucose control or acutely

severe symptoms (Parrish, 2015).

ACG guidelines recommend a trial of nasojejunal feeding prior to the placement of

jejunostomy tube for three days to ensure that at least 80 mL of enteral nutrition can be delivered

per hour, as this rate is essential if jejunal feeding is to succeed in the long term. Keeping a

jejunal tube in an appropriate position can be a challenge, however, particularly in patients with

persistent vomiting. Direct jejunostomy placement can also mitigate the likelihood of tube

displacement but is relatively more technically challenging and precludes the possibility of

gastric venting. Patients on enteral feeding are permitted small-volume liquid meals by mouth

during the day. A nutrient formula should be selected in consultation with an expert in nutrition,

and guided by the individual patient's caloric, fat, protein, and supplement needs, caloric density

and osmolality of the formula (Camilleri et al., 2013).

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NUTRITIONAL APPROACHES TO GASTROPARESIS
Parenteral nutrition should be restricted to patients with severe gastric and small intestinal

dysmotility who have failed enteral nutrition with prokinetics and antiemetic therapy. Parenteral

nutrition is seldom necessary in patients with gastroparesis, unless it is part of a generalized

motility disorder (Warner & Jeejeebhoy, 1985).

Conclusion

In summary, initial management of gastroparesis consists of dietary modification,

optimization of glycemic control and hydration, and in patients with continued symptoms,

pharmacologic therapy with prokinetic and antiemetics. Enteral supplementation is preferred

when oral nutrition is deemed inadequate, with post-pyloric feedings perhaps easier to rationalize

in the setting of documented gastroparesis. Foods that have been identified to aggravate in

gastroparesis, avoidance of these foods can be considered on observation and experiment basis.

Further studies are required in the areas of nutrition support and overall dietary management to

make the evidence stronger.

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