Gastroparesis and nutrition

Chapter 3.6
Gastroparesis and nutrition

Richard Keld¹ and Simon Lal²

¹Wrightington, Wigan and Leigh NHS Foundation Trust, Wigan, UK

²Salford Royal NHS Foundation Trust, Salford, UK

Gastroparesis is defined by delayed gastric emptying in the absence of mechanical obstruction. In health, gastric emptying is governed by rhythmical ‘slow waves’ of peristaltic contractions of the smooth muscles in the gastric fundus, body and antrum [1]. This activity is initiated in the gastric ‘pacemaker cells’ or interstial cells of Cajal and is under vagal control. In gastroparesis, perstaltic contractions are reduced by loss of the gastric pacemaker cells [2,3] and/or disruption of the vagus nerve, culminating in one or more abnormalities in gastric motility such as hypomotility, gastric arrhythmia and/or lack of antropyloroduodenal propagation [4]. In the USA, the prevalence of gastroparesis is 1 per 10,000 males and 4 per 10,000 females [5]. However, this may be an underestimate since delayed gastric emptying is thought to occur in up to 50% of patients with diabetes mellitus [6,7] and up to 50% of patients with functional dyspepsia [8] (also known as non-ulcer dyspepsia) or irritable bowel syndrome.

3.6.1 Factors involved in causation

The most common cause of gastroparesis, accounting for up to 50% of cases, is idiopathic [9]. Here the underlying cause is unclear, although a large proportion of patients have a history of viral infections [10,11] and psychological stress [10]; as such, there may be an overlap with functional dyspepsia [8]. The second most common cause of gastroparesis is diabetes mellitus, accounting for up to 30% of cases [9]. Typically, patients also display evidence of an autonomic neuropathy with postural hypotension and cardiac arrhythmias [12]. Postsurgical gastroparesis accounts for up to 13% of all cases of gastroparesis and can occur as a complication of gastric, oesophageal, duodenal or pancreatic surgery following disruption of the vagus nerve [9].

Proton pump inhibitor therapy has significantly reduced the frequency of gastric surgery (for peptic ulcer disease), but this trend is being reversed as a result of the obesity epidemic. The obesity epidemic is accounting for a resurgence of gastric surgery and this is likely to increase the frequency of postsurgical gastroparesis in future years.

Additional causes of gastroparesis are pharmacological, including tricylic antidepressants and opiate analgesics, and multisystem disorders including Parkinson’s disease and systemic sclerosis [5].

3.6.2 Dietary effects of disease or its management

Symptoms of gastroparesis typically consist of nausea and/or vomiting, occurring in 74% and 53% of all patients respectively; additional symptoms include abdominal pain, bloating, early satiety, postprandial fullness and weight loss [5]. Of course, this constitution of symptomatology is not specific and is insufficient to clinch a diagnosis of gastroparesis, but in high-risk groups, such as patients with diabetes and those with functional dyspepsia, a low index of suspicion should prevail.

Gastroparesis is not only varied in its aetiology but also in severity. Nutritional intake can be significantly compromised, resulting in weight loss, vitamin and mineral loss and dehydration, necessitating hospitalisation in severe cases [13,14]. Gastroparesis is classified by severity according to the Gastroparesis Cardinal Index Score which takes into account all the aforementioned factors and is a useful tool to guide treatment options [15].

3.6.3 Investigations

The diagnosis of gastroparesis can be suspected after normal standard diagnostic endoscopic and radiological investigations that have excluded a mechanical gastric outlet obstruction. Although there are many different modalities for diagnosing gastroparesis (reviewed in Keld et al. [16]), food residue seen on gastroscopy despite a 12-h fast may be an important clue. Scintigraphy is the gold standard to confirm the diagnosis and involves ingestion of a standardised radiolabelled meal containing technetium-99 or indium-111, after an overnight fast. To avoid variation in measurements between laboratories, the Neurogastroenterology and Motility Society and the Society of Nuclear Medicine have recently recommended using a standardised egg-white meal (eggs, two slices of white bread, strawberry jam (30 g), water (120 mL), and technetium-99m sulphur colloid, 0.521 mCi) (Egg Beaters^®) [17]. The test is deemed positive if more than 60% residual ingested meal content is detected within the stomach after 2 h, or more than 10% residual content is detected at 4 h [18].

3.6.4 Dietary treatments

Treatment strategies in gastroparesis aim to improve symptoms and reduce nutritional impairment, ideally by improving gastric emptying. Dietary therapy is central to disease management in all cases, although the evidence basis for dietary manipulation solely derives and is extrapolated from research in healthy subjects, not patients with gastroparesis. Alternative treatment strategies include pharmacological therapy, including antiemetics, prokinetics and botulinum toxin (reviewed in Keld et al. [16]), but the evidence basis and response to this approach are also limited [19–22]. Recently, the development of implantable gastric pacemakers shows promise in severe cases of gastroparesis, but this intervention is still under scrutiny and not widely available [23].

A detailed dietary history should focus on the type and consistency of foods tolerated and the timing, content and size of meals in relation to symptoms. Evaluation of nutritional and fluid status (including weight and anthropometric measurements), glycaemic control and the presence of any vitamin and mineral deficiency is also needed.

Food consistency

In health, non-nutrient liquids have fast gastric emptying times of 20 min and, when plotted on a graph, gastric emptying times are exponential [24]. Nutrient-containing liquids have slower emptying times and display a linear plot, and solid foods are slower still due to an initial plateau as a consequence of the grinding of food particles; this is termed the lag phase [24]. Similarly, in patients with gastroparesis, the gastric emptying time for small food particle size (e.g. blended carrots) is quicker than that of a large food particle size (e.g. chopped carrots) [25]. Small food particle sizes have a reduced lag phase of gastric emptying. In view of this change in physiology, simple manipulation of food consistency can be very effective in the management of gastroparesis. In mild cases adequate chewing may be sufficient to reduce food particle size while in moderate to severe cases, a puréed or liquid diet may be required.