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Frequently asked question: What is gastroparesis?

Written by Loren Buhle and Jim Reed

Last updated 27June96: Added section written by Loren Buhle

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[The following section was written by E. Loren Buhle, Jr., Ph.D.]  

Gastroparesis is the eventual paralysis of the GI system. Neuropathy...
stoppage or incorrect functioning of the autonomic nervous system 
(enteropathy). The result is a cessation of gastric motility...meaning 
food tends to sit in your intestines for a long time. Your stomach may 
have delayed emptying...meaning your stomach feels full of your 
breakfast when you sit down to dinner/supper. Additionally, there may be 
disturbances in the release of gut hormones and other metabolic 
abnormalities that also alter the GI motility. The typical symptoms are 
anorexia, nausea, vomiting, and abdominal pain.

Gastroparesis is detected in about 25 percent of people with DM. 
Although it is clinically silent in most patients, severe diabetic 
gastroparesis is the most debilitating of all the GI complications of 
diabetes. Liquid emptying is controlled by the proximal stomach (fundus) 
and is dependent on the volume of gastric contents. Solid-phase emptying 
is determined by powerful circular contractions of the distal stomach 
(antrum). These contractions grind and mix solid food into particles 
less than 1mm in size, so they may pass through the pylorus into the 
duodenum. Particles too large to escape through the pylorus during the 
postprandial period must be emptied during the stomach's interdigestive 
phase. During periods of fasting, a coordinated wave of activity, known 
as the migrating motor complex (MMC), sweeps through the stomach and 
small bowel every 90 minutes or so to clear the gut of indigestible 
debris and prevent bacterial overgrowth.

With diabetic gastroparesis, normal antral contractility is lost; 
therefore, there are particular problems with solid-food emptying. Loss 
of gastric MMC activity also occurs, leading to gastric statis and 
possible bezoar (collection of fibers, hair, and other indigestible 
matter...think hairball) formation. Some individuals also experience 
prolonged pylorospasms, which further impairs gastric emptying.

Symptoms again:
- nausea
- vomiting
- early satiety
- abdominal bloating
- epigastric pain
- anorexia

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[The following section was written by Jim Reed.]

Gastroparesis sufferers may experience any or all of the following: 
nausea, vomiting, early satiety (you feel full almost immediately after 
starting to eat), abdominal bloating, epigastric pain, and sometimes 
anorexia. With gastroparesis, you can often burp food that you consumed 
many hours previous or even throw it up. Sometimes the nausea may be 
delayed, but more frequently it happens soon after eating. At times the 
nausea and vomiting can become so bad that hospitalization may be 
required. That is often why anorexia can be a factor. Since food may not 
be properly digested, the person simply chooses not to eat rather than 
be sick all the time. Obviously that doesn't work out in the long run.

The stomach has several areas, and as the digestion process occurs, food 
moves through it via powerful contractions (the proximal stomach 
[fundus] controls liquid emptying, and the distal stomach [antrum] 
controls the emptying of solids). Food is ground up to about 1mm-sized 
particles and mixed with digestive juices. It then passes from the 
pylorus and into the duodenum. There are other contractions that take 
care of larger sized particles and migrating motor waves that sweep 
through the stomach during fasting periods to "clean it out." With 
gastroparesis, the normal movement of food is lost, at least some of the 
time, because of damage to the nerves involved in the digestive process.  
As a result, food sits undigested and results in great discomfort for 
the individual experiencing the problem.

For those people with gastroparesis who also take insulin and, 
presumably, oral agents, there can be substantial problems with hypo-
and hyperglycemia. With the process of food delivery to the small bowel 
interrupted, there can be real problems from the previous delivery of 
insulin to the body but with no food available to cover it. Often later, 
when digestion does occur, then the person is faced with hyperglycemia 
since now the body has food but little or no insulin to cover it. This 
can and does result in wide swings in blood glucose. As an example, my 
last 90 day average for bg's was 124 mg/dl but my HbA1c was 8.6! Like 
many people with gastroparesis, I never know if it will be a factor 
today or not. Gastroparesis is very often inconstant. I may or may not 
digest food within the correct timeframe. I can't tell prior to eating 
if it will "strike" or if my food will be digested normally. That makes 
planning of exogenous insulin delivery very difficult. I have noted that 
the higher in fat my food, the greater will be the probability of 
significantly delayed stomach emptying.

There can exist gastrointestinal tract disorders in upwards of 75% of 
diabetics. Not all diabetics experience the problems and not all 
diabetics with gastrointestinal problems (encompasses the entire 
digestive tract from the esophagus to the anorectum) are aware of the 
problems they do have. Perhaps 25% of longer-term diabetics have some 
level of gastroparesis, although it can also be silent even though it 
is present. Routinely, other gastrointestinal problems should be 
considered before a diagnosis of gastroparesis is determined. These may 
include cancer, severe gastritis, ulcers, or gallstones. Tests can 
include nuclear solid-phase emptying studies, "scope" tests, or upper-GI 
barium series tests. Treatment for gastroparesis may include the use of 
a variety of pharmacological agents such as Metoclopramide, Bethanecol, 
Domperidone, Cisapride (becoming quite popular, such as Propulsid), and 
Erythromycin. Glucose control is also very important since hyperglycemia 
increases the problem and exacerbates it. Other gastro-related problems 
with which diabetics face increased risk include severe 
gastritis/hemorrhagic gastritis, gallstones (although it is not certain 
that the increased risk is anything more than incidental), pancreatic 
insufficiency, diabetic diarrhea, fecal incontinence, and constipation.