Gastroparesis (part 2)

Groombridge Place, June 2013

In part 1, I described the symptoms of gastroparesis, what might be causing it in someone with diabetes, and the problems that arise - gastrointestinal symptoms, poor glycaemic control, malnutrition and weight loss, and depression. Now I'm going to write about possible treatments.

Nerve damage, if that's what is causing the problem, is irreversible. We can't (yet) mend nerves: once they're gone, they're gone. There doesn't seem to be an option to fix the faulty pacemaker cells either. But it is always useful to run through a list of things that will definitely not be helping. For example, opiate drugs are known for their constipating effects, and should be replaced with alternative painkillers if pain relief is necessary. Cigarette smoking has been shown to delay the gastric emptying of solids. Unfortunately, high blood sugar has also been shown to significantly delay gastric emptying, which is of no comfort to the person with diabetes who has been trying unsuccessfully to manage wild swings in blood sugar in the face of unyielding opposition from the gastroparesis itself. So I wouldn't bother opening that particular can of worms.

There are three methods used to help improve gastric emptying: pharmacotherapy (i.e. drugs), diet and surgical approaches. Two types of drugs can help with symptoms: prokinetics, which help to speed the intestinal contents on their way, and anti-emetics, which are used to prevent nausea and vomiting. These are routinely used, but changes to diet can be more effective than the medicines.

The Glycaemic Index (GI) is often used to assist with blood glucose control and weight management, and describes the speed at which carbohydrates are digested. High GI foods e.g. foods containing large proportions of monosaccharides and disaccharides (sugars) are digested quickly, and their glucose payload can reach the bloodstream before subcutaneous insulin has had time to get there, causing blood glucose to rise beyond the desired range. Low GI foods (complex starchy carbohydrates) such as oats and pulses are digested more slowly, and therefore deliver glucose to the blood slowly and more controllably, and keep you feeling fuller for longer. Unlike the majority of people with diabetes, high GI foods may help someone with diagnosed gastroparesis. These foods tend to contain simple sugars or processed carbohydrate and little fat and fibre - sweets, white bread, mashed potato.

Another good reason to avoid fibre, apart from its role in slowing gastric emptying, is that as it hangs around in the stomach it can contribute to the formation of unwanted fibrous masses called bezoars. The disadvantage of avoiding fat, however, is that someone with chronic gastroparesis is at risk of malnutrition, and could do with the calories supplied by energy-dense fatty food.

The diabetologist who referred the patient with gastroparesis to me suggested that a low carbohydrate diet might help reduce the volatility in blood glucose levels. The problem with this approach is that taking out the carbs leaves an energy deficit that can either be filled by protein or fat. Protein increases feelings of satiety, which is certainly not what we want, and fat slows gastric emptying. Blood glucose levels may be better managed with a greater proportion of high GI carbohydrate, which might actually be released from the stomach in a more predictable manner.

Research suggests other dietary recommendations, both to relieve symptoms and to maintain nutritional status. Small frequent meals are digested better than three large meals a day, and 'particle size' makes a difference - food should be chewed well, and liquids seem to leave the stomach more easily than solids. A patient might be prescribed three liquid supplements a day, adding a much needed 900 calories. Positioning during a meal, and sitting up and/or walking post-meal can promote gastric emptying; alcohol and carbonated drinks tend to exacerbate symptoms of bloating.

Placing a feeding tube below the stomach and pylorus in the jejunum (upper small intestine) allows nutrition to bypass the problem area, but brings with it the risk of infections and the inconvenience of having to be hooked up to a feed pump for hours at a time - jejunal feeding has to be much slower than feeding into the stomach. If nutritional status continues to decline, intravenous (parenteral) feeding is a possibility, but brings a whole new range of potential complications.

As well as addressing symptoms and nutrition, there are those pesky blood sugars to consider as well. Eating a meal containing carbohydrate requires a matching dose of insulin in order to maintain blood glucose within the desirable range, but we have seen that giving the insulin at the usual time (before, during or immediately after the meal) doesn't work if the glucose hits the bloodstream over a period greater than the lifetime of the insulin. So we could try splitting the insulin dose, perhaps giving 30% of the total dose just after eating, and the remaining 70% after an hour, or two, or whenever we think blood glucose is rising.

If you don't want to end up as a pincushion, this type of insulin regimen can be managed much more comfortably and conveniently with an insulin pump, which can be programmed to deliver insulin at whatever rate you desire. Delivering 6 units of insulin at one-tenth of a unit every five minutes over five hours can't be done with conventional insulin injection devices, but is a piece of cake with a pump.

Unfortunately the NHS doesn't fund Continuous Glucose Monitoring (CGM) systems, which have a subcutaneous sensor that samples interstitial fluid every five minutes linked to a device that translates the reading into an estimated blood glucose level. We lend these systems to patients to wear for just seven days at a time when we can't work out what their blood glucose is doing. Otherwise, users have to buy the kit and consumables themselves, which works out rather expensive. Although not mentioned in the research papers I have read about this condition, I think that CGM in combination with an insulin pump would be a valuable and effective approach to managing blood glucose with gastroparesis.

Finally, there are more technical and innovative options to try.

• Gastric electrical stimulation (GES) was approved in 2000 in the USA. Similar to a heart pacemaker, the GES device is implanted next to the stomach and mimics the role of the gastric pacemaker cells, stimulating and enhancing vagal function and muscle tone. 
• Botox (Clostridium botulinum toxin) is a muscle relaxant used cosmetically to reduce facial wrinkles, but will relax muscles elsewhere to therapeutic effect. Injecting Botox into the pyloric sphincter may cause it to relax sufficiently to allow better gastric emptying, but trials have shown this effect to be short-lived. 
• In future, that universally-cited panacea 'stem cell therapy' may be relevant, providing a way to replace or rejuvenate those faulty pacemaker cells of Cajal.