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Date of last update: 10/15/2017.

Forum Name: Gastroenterology Topics

Question: Long Term Stomach Fullness after eating

 apdco2 - Tue Jul 27, 2010 11:09 pm

I have suffered from Stomach Fullness after eating or drinking anything. This has been going on now for about 8 months. I have had every test that you can think of done and everything comes back "clear" I have had endoscopy's, Colonoscopy, upper and lower GI, xray's , Ct Scans. So far the only thing my GI Dr has done is give me pills for acid reflux ( which is not doing anything for me ) Recently while in for an ultrasound they noticed small polyops on my gallbladder so they took it out and the dr stated " we hope this helps your stomach problems also"... it did not.
I was cheacked for Chron's disease but it came back neg. Liver Function panel came back normal with slightly elevated protein levels but nothing to worry about
I am really at the point where i am so frustrated because i'm tired of living with this and i need some answers... Can anyone please help
 Dr.M.Aroon kamath - Thu Jul 29, 2010 11:34 pm

User avatar Hi,
In your case, as most of the standard testing has been gone through and as yet there is no lead, one is compelled to consider the more uncommon and rare causes of bloating of the stomach such as,
- Gastroparesis,
- bezoars,
- Idiopathic slow-transit constipation - a pangastrointestinal dysmotility disorder,
- Adult hypertrophic pyloric stenosis,etc.

Gastroparesis is an as yet not fully understood entity. It is one among the dysmotility disorders.

Some studies indicate that gastric contractions are generated by slow waves in the smooth muscle, which occur in the absence of neural activity and are thus believed to be myogenic. This myogenic activity in the digestive tract is believed to originate in the interstitial cells of Cajal (ICC), which act as pacemakers, generating slow waves in the smooth muscle, which then travel all the way down to the large gut in between meals.The autonomic system perhaps modulates the gastric peristaltic activity.

There is considerable normal variability among healthy people in transit times through different sections of the gatrointestinal tract. Secondly, the time required for material to move through the digestive tube is significantly affected by the composition of the meal. Finally, transit time is believed to be influenced by such factors as psychological stress, gender and reproductive status.

Gastric dysmotility can be
- transient/occasional, or
- chronic.

Occasional gastroparesis: related to consumption of fatty and rich foods, excessive alcohol, eating late at night, irregular food intake etc.
Transient dysmotility: seen sometimes during any acute illness including postviral syndromes(ex; viral gastroenteritis).
Chronic gastroparesis: nearly one third are Idiopathic (gastroparesis with no known cause).Some of the ther causes are,
- diabetic autonomic neuropathy, a common cause, associated with both type 1 or type 2 diabetes of long duration.
- autoimmune diseases and syndromes, such as fibromyalgia and Parkinson's disease.
- disorders of smooth muscle , such as amyloidosis and scleroderma.
- metabolic disorders, including hypothyroidism,
- endocrine disorders such as hypoadrenalism secondary to hypothalamic-pituitary dysfunction.
- some mitochondrial disorders.
- due to anorexia nervosa, bulimia and other eating disorders.
- a number of drugs may interfere with gastric motility.
- post surgical gastroparesis(ex; following vagotomies),and
- bezoars: concretions that develop in the stomach, which can be a result or cause of gastroparesis.

Common symptoms of gastroparesis: are fullness after just a small amount of food, abdominal bloating, loss of appetite, heartburn, GERD, fluctuating blood sugar levels, and malnutrition.

Diagnosis of idiopathic gastroparesis is possible only after excluding other causes.The various diagnostic modalities available are
- gastric emptying studies: one of the most accurate ways to diagnose gastroparesis. The most commonly used is radioisotope gastric-emptying scan.
- a barium 'beefstake' meal follow through study,
- a gastro duodenal manometry,
- an Upper GI endoscopy,
- MRI is also being used to evaluate the motility of the stomach.

Management: firstly, any underlying etiological factors must be treated as needed.

Dietary management: aimed at speeding up the gastric emptying. Generally,larger a meal, the slower the gastric emptying will be. Therefore, reducing the meal size and increasing the frequency (small 6-8 meals or more if necessary) helps. Another useful strategy is to replace solid-type calories with with more of liquid-type calories. This regimen is continued for a while and then gradually one can switch over to puréed foods.Fiber restriction is not advisable unless a patient has or has had a gastric bezoar. Fat may(in some) slow gastric emptying. In such individuals, fat in the liquid form (such as liquid nutritional supplements,whole milk, milkshakes,and the like)often works well. Abolishing fat from the diet is not advisable as fat is a good calorie source and these patients are often malnourished.

Other modalities:
- Pharmacological -anti-emetics and prokinetics,
- newer modalities that are being tested are Botulinum (Botox) toxin injections into the pyloric musculature, and electrical gastric stimulation.

Surgical option: Occasionally, when all other approaches fail and the patient continues to remain severely malnourished, it may be necessary to perform a 'feeding jejunostomy'.
Some surgeons have used a new technique (Implantable gastric electric stimulation), wherein, a device, known as a "gastric neurotransmitter" is surgically implanted to control nausea and vomiting.

Adult hypertrophic pyloric stenosis: The etiology of adult IHPM is unclear.This entity is classified into
- a primary type (with no apparent underlying disease): thought to be due to the persistence of the juvenile into adult life.

- a secondary type (caused by pthologies such as carcinoma, excessive fibrosis during healing of a previous gastric or duodenal ulcers, gastrointestinal stromal tumors, bezoars, postoperative adhesions, and persistent vagal hyperactivity leading to pyloric muscular hypertrophy.

Other causes sporadically reported are postinflammatory complication in Crohn’s disease and duodenal mucosal diaphragm.

In your case, the duration of symptoms may not be considered “too long”
(8 months rather than years). So your doctor presumably may be justified in persisting with conservative measures(dietary +/- pharmacological), before considering other options (only if symptoms continue to persist or unfortunately worsen).Your nutritional status also must be assessed carefully.

I do hope that this turns out in the end as a temporary gastric dysmotility and that conservative measures will be successful.
Good luck!

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