Gastroparesis | Cedars-Sinai

Not what you’re looking for?

What is gastroparesis?

Gastroparesis is a stomach disorder. It happens when your stomach takes too long to empty out food.

If food stays in your stomach for too long, it can cause problems. The food can harden into solid masses. These are called bezoars. These masses may upset your stomach and make you vomit. They can also create a blockage in your stomach. This can be dangerous if it stops food from passing into your small intestine.

In most cases, gastroparesis is a long-term (chronic) condition.

What causes gastroparesis?

Gastroparesis is caused when your vagus nerve is damaged or stops working. The vagus nerve controls how food moves through your digestive tract. When this nerve doesn’t work well, food moves too slowly or stops moving.

The vagus nerve gets damaged if you have diabetes and your blood sugar or blood glucose levels stay high over a long period of time.

Other causes of gastroparesis include:

• Eating disorders, such as anorexia or bulimia
• Surgery on your stomach or vagus nerve
• Extreme tiredness that does not seem to be caused by a health problem (chronic fatigue syndrome)
• Some
  medicines that slow movement in your intestine, such as narcotics for chronic pain
• Disorders involving smooth muscle that may affect the stomach, such as amyloidosis and scleroderma
• Nervous system disorders such as abdominal migraine and Parkinson’s disease
• Metabolic disorders, which make the body have either too much or too little of
  essential things it needs to stay healthy, such as having too little of the thyroid
  hormone ( hypothyroidism)
• A viral
  illness, such as a viral gastroenteritis

Who is at risk for gastroparesis?

You are more likely to have gastroparesis if you have type 1 or type 2 diabetes.

What are the symptoms of gastroparesis?

Each person’s symptoms may vary. Symptoms may include:

• Upset stomach or nausea
• Vomiting
• Weight loss
• Feeling full too soon after you start eating
• Belly (abdominal) bloating or pain
• Heartburn or GERD (gastroesophageal reflux disease)

The symptoms of gastroparesis may look like other health problems. Always see your doctor to be sure.

How is gastroparesis diagnosed?

Your healthcare provider will give you a physical exam and ask about your past health. He or she may also use other tests, including:

• Blood tests. These tests check your blood
  counts and measure your chemical and electrolyte (mineral) levels.
• Upper GI (gastrointestinal) series.This is also called a barium swallow. This test checks the organs of the top
  part of your digestive system. These are your food pipe (esophagus), your stomach,
  and the first part of your small intestine (duodenum). You will swallow a metallic
  fluid called barium. Barium coats the organs so that they can be seen on an X-ray.
  X-rays are then taken to check your digestive organs.
• Radioisotope gastric-emptying scan.During this test, you will eat food containing a mildly radioactive substance,
  or radioisotope, that will show up on a scan. The amount of radiation is very small.
  It is not harmful. But it lets the radiologist see the food in your stomach during
  the scan. He or she can also see how quickly food leaves your stomach. This test can
  take as long as 4 hours.
• Gastric manometry (antroduodenal manometry).This test checks the muscle movement in your stomach and small intestine. A thin
  tube is passed down your throat into your stomach. This tube has a wire that measures
  the muscle movement of your stomach as it digests foods and liquids. This helps show
  how your stomach is working. It also shows if your digestion is slower than
  normal.
• Upper endoscopy.This is also called esophagogastroduodenoscopy (EGD). This test looks at the
  lining or inside of your esophagus, stomach, and duodenum. This test uses a thin,
  lighted tube, called an endoscope. The tube has a camera at one end. The tube is put
  into your mouth and throat. Then it goes into your esophagus, stomach, and duodenum.
  Your healthcare provider can see the inside of these organs. He or she can also take
  a small tissue sample (biopsy) if needed.
• Wireless capsule study. This test involves
  swallowing a wireless capsule that measures stomach emptying and how fast food and
  fluids move through your intestine. You will pass the capsule out of your body with a
  bowel movement.
• Gastric emptying breath test (GEBT). This
  test checks stomach emptying by measuring how much carbon dioxide you breathe out
  over several hours after eating food.
• Scintigraphic gastric accommodation.This test measures your stomach contents before and after a meal. It also checks
  how well your stomach relaxes after you eat food.

How is gastroparesis treated?

In
most cases gastroparesis is a long-term or chronic health problem. It can’t be cured.
But you can manage the disease with a care plan.

If
you have diabetes and gastroparesis, the main goal is to control your blood sugar
levels. Any medicines that can cause gastroparesis will likely be stopped.

Treatment will depend on your symptoms, age, and general health. It will also depend on
how severe the condition is.

Your
care plan may include:

• Taking medicines.Your healthcare provider may prescribe a few medicines to see which works
  best.
• Changing your diet.Changing your eating habits can also help control the disease. In some cases
  eating 6 smaller meals a day is more helpful than eating 3 larger ones. Some experts
  suggest having a few liquid meals a day. They suggest you do this until your blood
  glucose levels are stable and your gastroparesis is under control. You may also be
  told not to eat fatty and high-fiber foods. These can slow your digestion and be hard
  to digest. See your healthcare provider or a dietitian for the eating plan that is
  best for you.
• Surgery.In some cases you may need a type of surgery called a jejunostomy. A feeding
  tube is inserted through the skin on your abdomen into your small intestine. This
  tube lets nutrients go right into your small intestine instead of your stomach. This
  surgery is used only if your gastroparesis very severe.
• Gastric neurotransmitter. This device may
  help control any upset stomach and vomiting. It is put into your body by
  surgery.
• Feeding by IV (intravenously).This is also called parenteral nutrition. This is when nutrients are put right
  into your veins. This is done instead of eating and having food go through your
  digestive system. A tube or catheter is put into one of your chest veins. The tube
  has an opening on the outside of your skin. A bag with liquid nutrients or medicine
  is joined to the tube. The fluids go into your bloodstream through your vein.

What are possible complications of
gastroparesis?

Gastroparesis can cause other health problems because food moves too slowly through your stomach. These health problems include:

• Having a hard time managing your blood sugar if you have diabetes
• Letting
  food sit too long in your stomach
• Having hard masses of food (bezoars) build up in your stomach. These can cause upset stomach, vomiting, and block food from passing into your small intestine.
• Losing too much weight and not getting enough nutrients (malnutrition)

Living with gastroparesis

Gastroparesis can lead to weight loss and not getting enough nutrients (malnutrition). It is very important to follow your health care provider’s diet instructions.

In most cases you will be given a special diet. This will have foods that are easier to digest and pass through your stomach. You may also be given medicines to take. Follow all instructions carefully.

When should I call my healthcare provider?

Call your healthcare provider right away if your symptoms get worse or if you have new symptoms. Problems such as a stomach blockage or high blood sugar need to be taken care of right away.

Key points about
gastroparesis

• Gastroparesis is a stomach disorder. It happens when your stomach takes too long to empty out food.
• If food stays in your stomach for too long, too much bacteria may grow.
• The food can also harden into solid masses (bezoars). They may upset your stomach or create a blockage in your stomach.
• In most cases gastroparesis is a long-term (chronic) condition.
• You are more likely to have it if you have type 1 or type 2 diabetes.
• Symptoms may include upset stomach or nausea, vomiting, losing weight, feeling full too soon when eating, belly or abdominal pain or bloating, and heartburn.
• Your care plan may include taking medicines, changing your diet, having surgery, and feeding by IV (intravenously).
• Treatment will not cure gastroparesis, but it can help you manage the disease.

Next steps

Tips to help you get the most from a visit to your healthcare provider:

• Know the reason for your visit and what you want to happen.
• Before your visit, write down questions you want answered.
• Bring someone with you to help you ask questions and remember what your provider
  tells you.
• At the visit, write down the name of a new diagnosis, and any new medicines,
  treatments, or tests. Also write down any new instructions your provider gives
  you.
• Know why a new medicine or treatment is prescribed, and how it will help you. Also
  know what the side effects are.
• Ask if your condition can be treated in other ways.
• Know why a test or procedure is recommended and what the results could mean.
• Know what to expect if you do not take the medicine or have the test or
  procedure.
• If you have a follow-up appointment, write down the date, time, and purpose for that
  visit.
• Know how you can contact your provider if you have questions.

Medical Reviewer: Raymond Kent Turley BSN MSN RN

Medical Reviewer: John Hanrahan MD

Medical Reviewer: L Renee Watson MSN RN

© 2000-2021 The StayWell Company, LLC. All rights reserved. This information is not intended as a substitute for professional medical care. Always follow your healthcare professional’s instructions.

Not what you’re looking for?

A Mysterious Stomach Disorder That’s on the Rise in Teenage Girls and Women in Their 20s – Health Essentials from Cleveland Clinic

“Doc, I don’t have an eating disorder,” a young woman with a slight frame tells her gastroenterologist. “I have disordered eating.”

Cleveland Clinic is a non-profit academic medical center. Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services. Policy

And in a growing number of teenage girls and women in their 20s, it’s true. They suffer from a mysterious stomach disorder called gastroparesis, in which the stomach can’t empty normally.

“Every time they eat, they get sick,” explains gastroenterologist Michael Cline, DO, of Cleveland Clinic’s Gastroparesis Clinic. “So they don’t want to eat.” The most common symptoms: nausea, vomiting, abdominal pain, feeling full, bloating. Who can blame them?

Gastroparesis literally means “paralyzed stomach” — “gastro” means stomach and “paresis” means paralyzed.

“When the stomach doesn’t do its job grinding up food, you don’t get nutrition out of it,” Dr. Cline explains. “And if food sits there too long, it typically comes back up through vomiting.”

A rapid increase in diagnosis

While it’s not yet known how many are affected or why, Dr. Cline says gastroparesis has surged in young women in the U.S. since 2014. The number of young women he treats with gastroparesis now doubles each year.

This has thrown those who treat gastroparesis a curveball. Up until that point, sufferers were evenly split between those with diabetes and idiopathic cases — meaning those with no known origin, he says.

“In these young women, it tends to be autoimmune-related,” Dr. Cline says. Many have thyroid disease, rheumatoid arthritis or lupus.

Why it’s a mystery that’s hard to crack

“We screen these girls’ and young women’s blood for autoimmune disease and find all kind of weird — and they really are weird — antibodies to the nerves and muscles,” Dr. Cline says. One of them is called GAD, or glutamic acid decarboxylase. It’s more common in type 1 diabetics. But in a nondiabetic, it’s significant.

Other odd finds? Potassium channel, sodium channel and myasthenia antibodies. These irregularities are found using a blood panel test called an autoimmune GI dysmotility (AGID) diagnostic panel.

Antibody testing? Check. But then come physical tests that check how someone’s GI tract is moving. Dr. Cline says one main problem in properly diagnosing gastroparesis is that an EGG test alone — that’s an electrogastrogram — isn’t enough to make sure whatever problem the patient has is really gastroparesis.

Not all ‘gastroparesis’ is gastroparesis

“There’s a lack of general motility (how things move along) testing,” Dr. Cline explains. “These patients get labeled with gastroparesis with just one test. But we need to look at the entire intestine too.”

There’s plenty of other motility disorders that can masquerade as gastroparesis. The most common? Slow transit colon — that’s constipation. And then there’s global dysmotility, where the entire gut doesn’t move. Or, rarely, it’s only the small intestine that doesn’t work.

“It’s best to take five steps backwards and say, ‘I’m not sure you have gastroparesis yet. You sure give me a lot of symptoms of it. But what if we test your intestine and something else is wrong?’” he says.

The average time from first experiencing symptoms until proper diagnosis? Over 2 years.

The best test to definitively diagnose gastroparesis uses a “smart” pill you swallow to collect data from your GI tract, Dr. Cline says.

But … help IS available

In teens and young women who “purely” have gastroparesis, the first treatment Dr. Cline recommends is intravenous immunoglobulin (IVIg). Given weekly through IV for 12 weeks, this medication has been shown to help reduce vomiting, nausea, abdominal pain and bloating.

It works by fighting those odd, autoimmune-related antibodies off the nerves and muscles. But, he says, it’s astronomically expensive and often has to be repeated.

Unfortunately, there aren’t a lot of good motility drugs available, Dr. Cline notes. Metoclopramide (Reglan^®) and erythromycin are used, though sparingly as they’re not terribly effective.

An innovative POP procedure (that stands for per oral endoscopic pyloromyotomy) is one of the best new endoscopic approaches. It’s done under anesthesia through a scope that’s inserted through the mouth. And it has excellent results.

A look at how POP works

“We make a small cut in the lining of the stomach — over the top of the muscle that regulates how food gets out,” Dr. Cline says. “This allows food to actually empty.”

So how effective is it? Dr. Cline says Cleveland Clinic has a 70% success rate (a rate that’s so high since adequate testing is done to make sure patients truly have gastroparesis first). POP has largely replaced implantable gastric pacemakers for gastroparesis because it’s much less invasive, he adds.

“The pacemaker is a great idea in the right patient,” he says. “But the problem is, if doesn’t work, now you’ve got this device that’s screwed into the stomach. So we start with the least invasive approach.”

What if it’s really not gastroparesis?

Treating a patient for gastroparesis, if it’s not gastroparesis, won’t help.

“If the problem is the colon, we can typically get that moving with medication,” Dr. Cline says.”If it’s both the colon and stomach, we can use medication for the colon and POP for the stomach. ” But if the stomach, small intestine and colon are all slow, other medications available through Food and Drug Administration compassionate use programs are the best option.

The bottom line? “There is help,” reassures Dr. Cline. “But we have to figure out what’s wrong. It’s a lot easier to hit the target in the daylight than it is in the dark.”

Gastroparesis – American College of Gastroenterology

Overview

Gastroparesis is a chronic disorder which means delayed stomach emptying without a blockage. In healthy people, when the stomach is functioning normally, contractions of the stomach help to crush ingested food and then propel the pulverized food into the small intestine where further digestion and absorption of nutrients occurs.

Symptoms

Symptoms include fullness after meals, pain, nausea vomiting, weight loss, belching and bloating. Certain foods like fatty foods, or carbonation may cause symptoms. The feeling of fullness after starting a meal is very common. Weight loss may also occur.

Causes

Diabetes is one of the more common causes. Gastroparesis may also occur after stomach surgery. Other causes include bacterial and viral infections. Narcotics, antidepressants and other medications which delay stomach emptying may also cause gastroparesis. There are a group of patients with gastroparesis where there is no obvious cause.

Diagnosis

Gastric Emptying Studyis the most commonly used test. It is a test using a tiny amount of radioactive material mixed with food. With imaging equipment, it measures the rate of emptying of the stomach after taking a meal. A delay in gastric emptying indicates gastroparesis.

13 C spirulina Gastric Emptying Breath Test is a non radioactive test to evaluate for gastroparesis. It is a test also using labeled food where the patient provides breath samples for analysis.

Wireless capsule system called (SmartPill®)

Is a capsule that contains a small electronic device. This device records information as it travels to your stomach and intestine. The information is transmitted to a receiver worn on the waist. The capsule is passed in your stool.

Treatment

Importance of Nutrition as Treatment in Gastroparesis

The initial treatment in patients with gastroparesis is to create a diet that will improve the symptoms. Your physician may recommend eating frequent small meals and to avoid fatty, spicy, acidy and high fiber foods. Your physician may also recommend soups or more liquid containing meals.

In addition, we always want to make sure our patients are well hydrated.

Those patients with diabetes should have good control of their sugars.

Medicines that delay stomach emptying should be avoided if possible.

Metoclopramide

Is an important medicine to treat gastroparesis. There are risks in using this medication that you need to discuss with your physician. She will help you weigh the pros and cons and help you make the best decision for your situation.

Erythromycin You may know erythromycin as an antibiotic. Erythromycin also causes stomach contractions. Your physician may consider this option if you fail to respond to metoclopramide or you wish to try something else.
Erythromycin also has side effects. It does not work after 4 weeks. Your doctor will also help you weigh the pros and cons of using this medication.

Anti Emetics (Medications to control nausea and vomiting) Your physician may also consider the use of medications like prochlorperazine (Compro), diphenhydramine (Several brand names including Benadryl), ondansetron (Zofran). There are risks and benefits to these medications as well.

Special Treatments

G -POEM (gastric peroral endoscopic myotomy) is a specialized procedure done in those patients who have not responded to other therapies. It involves minimally invasive surgery of the stomach performed by endoscopy.
An endoscopy is a test that is performed after giving intravenous sedation. A small tube is inserted in the stomach where the surgery occurs.

There are additional experimental options that your doctor may discuss with you including surgically placing an electric stimulation device on your stomach. The electrical stimulation helps control symptoms.

There are several newer pharmacological agents on the horizon that offer promise in treating gastroparesis

Figure 1: Gastrostomy and jejunostomy anatomy

Figure 2: Oro-jejunal feeding tube

Figure 3: Wireless Capsule Monitoring System

Figure 4: Electrical Gastric Stimulation

Author(s) and Publication Date(s)

Jean Fox, MD and Amy Foxx-Orenstein, DO, FACG, Mayo Clinic, Rochester, MN, and Scottsdale, AZ – Published August 2004. Updated November 2008. Updated December 2012.

Return to Top

Gastroparesis — Gaudiani Clinic

 Written by Elissa Rosen, MD, CEDS for the Gaudiani Clinic Blog

In those who have restricted calories resulting in weight loss, whether in the setting of a clinically evident eating disorder or even with relative energy deficiency in sport (RED-S), movement of food and waste through the gastrointestinal (GI) tract can be slowed. The exact reason why this occurs is not entirely known though it is believed to be in part due to an attempt for the body to conserve energy during periods of low energy input. Delayed emptying of food from the stomach, also called gastroparesis, can lead to early fullness, bloating, abdominal distension, and nausea. (1) As you can imagine, trying to increase nutritional intake in the face of gastroparesis can be really challenging. Today, we are going to talk all things gastroparesis including symptoms, diagnosis, and treatment. Of note, there are many causes of gastroparesis, but today we are just focusing on gastroparesis that develops in the setting of decreased nutritional intake and weight loss.

Gastroparesis is felt to be nearly universal in those who have restricted calories resulting in significant weight loss (generally 10-20% of body weight). (1) It is worth emphasizing that gastroparesis can occur in those of all body shapes and sizes and one does not need to be clinically underweight to develop gastroparesis. (2) The most common symptoms are early satiety (meaning feeling very full even after just a small amount of food) and bloating. For those with an eating disorder, specifically those who have body image concerns that focus on the appearance of their abdomen, a distended and bloated stomach can certainly challenge even the most recovery motivated person.

Gastroparesis can be formally diagnosed through a specific study called a nuclear medicine gastric emptying study. During a gastric emptying study, a radioactive material is placed within a food (generally scrambled eggs or an egg substitute). Images of the digestive tract are taken at varying time intervals, usually with the last being 4 hours after the initial food ingestion. A radiologist will then read the images and determine what percentage of food remains in the stomach at each time interval. In those with gastroparesis, the amount of food retained at these intervals will be higher than those without delayed stomach emptying. Generally speaking, less than 10% of the food should be left in the stomach at the four-hour mark. (2) I have seen gastric emptying studies where nearly half of someone’s food still remained after four hours. It is easy to see why someone would feel incredibly full when their stomach is emptying this slowly! While a formal gastric emptying study can be helpful in certain clinical settings especially where the diagnosis is not clear, they are often not necessary in those with a clinical history of restriction, weight loss, and symptoms consistent with gastroparesis given delayed gastric emptying is felt to be very common in this setting. Instead, empiric treatments can be undertaken without imaging. If symptoms linger despite traditional treatments, a gastric emptying study may then be indicated.

The gold standard for the treatment of gastroparesis is increased caloric intake and weight restoration when necessary. There are also several dietary and medication options to help manage symptoms initially.  From a dietary end, liquids will more readily empty from the stomach than solid foods so incorporating liquid nutritional into a meal plan can prove very helpful in the early stages of the nutritional rehabilitation process. In addition, foods that are higher in fiber (fruits, vegetables, whole grains) are harder to digest and can increase fullness and bloating. Reduction in fiber intake for a time period can really make a difference. Lastly, eating 5-6 smaller sized meals throughout the day versus 3 larger meals will be much easier to tolerate.

From the medication front, there are several different medications that work on the stomach to promote gastric emptying. The goal of using medications is to help ease the barrier that gastroparesis can present during the nutritional rehabilitation process. Medications are only meant to be used short term, 1-3 months, while a person is doing the gold standard treatment (i.e., improved nutrition intake). Three different medications are commonly used and include metoclopramide, erythromycin, and azithromycin. For severe symptoms metoclopramide can be used in combination with erythromycin or azithromycin. (3) All three medications are generally well tolerated though they do have some noteworthy side effects that should be discussed prior to starting them. For example, both erythromycin and azithromycin are macrolide antibiotics that, taken long term, can decrease the healthy bacteria that exist in our intestines and allow for the growth of more harmful bacteria such as clostridium difficile which can lead to a severe diarrheal infection. The most serious side effects of metoclopramide are acute muscle spasms and facial twitches called tardive dyskinesia. All three medications can also cause prolongation of an interval on an electrocardiogram or ECG called the QTc interval, which when significantly prolonged can lead to arrhythmias. (3)

In conclusion, gastroparesis is a real medical complication that many people face in the setting of caloric restriction and weight loss no matter what one’s body shape or size is. These feelings of fullness and bloating are real and expert dietitians and physicians are able to help make the nutritional rehabilitation process easier in the setting of  gastroparesis.

1.     Mehler PS. Anderson AE. Eating Disorders: A guide to medical care and complications. 3rd edition. John Hopkins University Press. 2017.

2.     Gaudiani JL. Sick Enough: A guide to the medical complications of eating disorders. 1st edition. Routledge. 2019.

3.     Norris ML, Harrison ME, Isserlin L, Robinson A, Feder S, Sampson M. Gastrointestinal complications associated with anorexia nervosa: A systematic review.  Int J Eat Disord. 2016 Mar;49(3):216-37. doi: 10.1002/eat.22462. Epub 2015 Sep 26. Review. PubMed PMID: 26407541.

Effect of a Prokinetic Agent

Physiol Behav. Author manuscript; available in PMC 2013 May 15.

Published in final edited form as:

PMCID: PMC3314137

NIHMSID: NIHMS357070

Michael J. Devlin

^aColumbia University, Department of Psychiatry, 1051 Riverside Drive, Unit 116, New York, NY 10032, United States

Harry R. Kissileff

^bSt. Luke’s-Roosevelt Hospital Center, 1111 Amsterdam Avenue, New York, NY 10025, United States

Ellen J. Zimmerli

^aColumbia University, Department of Psychiatry, 1051 Riverside Drive, Unit 116, New York, NY 10032, United States

Francine Samuels

^aColumbia University, Department of Psychiatry, 1051 Riverside Drive, Unit 116, New York, NY 10032, United States

Benny E. Chen

^aColumbia University, Department of Psychiatry, 1051 Riverside Drive, Unit 116, New York, NY 10032, United States

Amanda Joelle Brown

^aColumbia University, Department of Psychiatry, 1051 Riverside Drive, Unit 116, New York, NY 10032, United States

Allan Geliebter

^bSt. Luke’s-Roosevelt Hospital Center, 1111 Amsterdam Avenue, New York, NY 10025, United States

B. Timothy Walsh

^aColumbia University, Department of Psychiatry, 1051 Riverside Drive, Unit 116, New York, NY 10032, United States

^aColumbia University, Department of Psychiatry, 1051 Riverside Drive, Unit 116, New York, NY 10032, United States

^bSt. Luke’s-Roosevelt Hospital Center, 1111 Amsterdam Avenue, New York, NY 10025, United States

Corresponding Author: Michael J. Devlin, MD, New York State Psychiatric Institute, Unit 116, 1051 Riverside Drive, New York, NY 10032, Telephone: (212) 543-5748, Fax: (212) 543-5607, ude.aibmuloc@5djmThe publisher’s final edited version of this article is available at Physiol BehavSee other articles in PMC that cite the published article.

Abstract

Objective

Previous studies have suggested that delayed gastric emptying and abnormal postprandial release of hormones that influence satiation, particularly cholecystokinin (CCK), may play an important role in the pathophysiology of bulimia nervosa (BN). This study was designed to test these hypotheses as well as the efficacy of the prokinetic agent erythromycin in patients with BN.

Method

Thirty-two normal weight women with BN and 24 control participants consumed a large liquid test meal. Gastric emptying and pre- and postprandial release of CCK, peptide YY (PYY), and ghrelin were determined. Participants with BN were then recruited for double-blind treatment with erythromycin up to 500 mg three times daily vs. placebo for six weeks, following which they consumed a repeat test meal with gastric emptying and appetitive hormone measurements.

Results

CCK release at 15 minutes following the meal was marginally lower(p = 0.1) in BN than in control participants. Rate of gastric emptying and postprandial hormone release were similar in BN and controls. BN patients assigned to erythromycin compared to those assigned to placebo had more rapid gastric emptying following treatment, but there were no differences in release of CCK, PYY, or ghrelin following the post-treatment test meal. Moreover, treatment with erythromycin was not associated with clinical response.

Discussion

The current study does not support the clinical utility of moderate dose erythromycin in treating BN. Furthermore, the findings suggest that a modest increase in gastric emptying rate is associated neither with altered postprandial hormonal release nor with clinical benefit in these patients. While providing no evidence for the effectiveness of prokinetic agents in this setting, our findings do not preclude the possibility that a greater increase in gastric emptying rate might prove beneficial.

Keywords: Bulimia nervosa, Eating laboratory, Eating disorders, Pharmacotherapy, Gastric emptying, Cholecystokinin

1. INTRODUCTION

The characteristic eating behavior of individuals with bulimia nervosa (BN), i.e. regularly occurring episodes of uncontrolled eating followed by vomiting or other forms of attempted compensation, may reflect an abnormality in the development of satiation over the course of a binge meal, particularly during its latter portion [1]. Investigations of the gastrointestinal physiology of individuals with BN have revealed abnormalities in postprandial release of cholecystokinin (CCK) and other appetitive hormones [2], gastric emptying [3,4], and gastric motility [5] following ingestion that may underlie the observed abnormality in satiation. We and others have proposed a model in which slowed gastric emptying contributes to decreased postprandial CCK release and blunted subjective sense of satiety, leading to uncontrolled overconsumption and possibly to compensatory purging [3,4,6]. The link between overconsumption and compensatory purging is at least in part attributable to overconcern with shape and weight, i.e. fear of weight-gain resulting from overconsumption, and the extreme discomfort that often follows binge eating [7]. If these behaviors directly or indirectly lead to further slowing of gastric emptying, a positive feedback loop may work to maintain the disorder.

This model suggests a crucial role for delayed gastric emptying in the causal chain that leads to maintenance of the disorder, and predicts that increasing gastric emptying in individuals with bulimia nervosa would be helpful in restoring normal satiation and in reducing binge-purge behavior. There has been one controlled study of the prokinetic agent cisapride for patients with anorexia nervosa, some with concurrent bulimic symptoms, that suggested at least a marginal effect of cisapride on subjective symptoms [8]. However, a definitive test of the model, particularly of the prediction that increasing gastric emptying would have therapeutic benefit in patients with bulimia nervosa, has not yet been conducted.

The current study was designed to assess the efficacy in patients with BN of a treatment that increases gastric emptying. We hypothesized that a medication that increased gastric emptying would: (1) partially or completely normalize postprandial appetitive hormone responses and (2) lead to clinical improvement over time. To increase gastric emptying, we used erythromycin, an antibiotic that is also an agonist of motilin and has been used to increase gastric empyting in patients with delayed gastric emptying due to gastroparesis in diabetes mellitus or postsurgical states [9]. We chose not to use cisapride due to its association with QT prolongation [10]. Additional aims of the study were to replicate previous findings regarding postprandial gastric emptying and CCK release in individuals with BN, and to examine postprandial release patterns of peptide YY (PYY) and ghrelin, appetitive hormones that have received relatively little study in these individuals [11,12].

2. MATERIALS AND METHODS

2.1 Participants

We recruited 32 normal-weight women with BN and 24 normal-weight female control participants matched for age and ethnicity. Participants with BN were recruited from the Eating Disorders Research Clinic at New York State Psychiatric Institute. All participants with BN met the following inclusion criteria: (1) DSM-IV criteria for BN [7] ascertained via the Eating Disorder Examination (EDE) [13] and clinical interview; (2) duration of BN at least 1 year; (3) purging via self-induced vomiting; (4) age 18–45 years; (5) 85–120% of ideal body weight. We excluded patients with major Axis I psychiatric disorders, ascertained via the Structured Clinical Interview for DSM-IV (SCID) [14], other than depression as well as those with recent suicide attempts. Patients taking antidepressant or other psychotropic medications known to affect appetite were excluded, as were patients whose depression warranted immediate treatment with antidepressants. We also excluded those with known intolerance to erythromycin, current pregnancy or lactation, unwillingness to use an effective method of birth control, or conduction delay on electrocardiogram. Normal-weight controls were recruited from the Columbia University and the Columbia Presbyterian Medical Center campuses, and were paid for their participation. All control participants met the following inclusion criteria: (1) no current or past psychiatric disorder; (2) 85–120% of ideal body weight for all of adult life excluding pregnancy based on 1959 Metropolitan Life Insurance standards [REF – See Zimmerli et al. , 2006, Ref #18]; (3) age 18–45 years; (4) no history of binge eating or self-induced vomiting. We excluded subjects who were taking medication, who had recent histories of abusing alcohol or other drugs, or who were medically ill. In addition to clinical interview, SCID, and EDE, baseline assessment included measurement of vital signs, completion of the Beck Depression Inventory (BDI) [15] and Eating Inventory (EI) [16] and, for BN patients, electrocardiogram. Recruitment of participants for this study was approved by the New York State Psychiatric Institute and St. Luke’s-Roosevelt Hospital Center Institutional Review Boards. The study is registered with ClinicalTrials.gov (NCT ID: {“type”:”clinical-trial”,”attrs”:{“text”:”NCT00304187″,”term_id”:”NCT00304187″}}NCT00304187).

2.2 Gastric Emptying and Appetitive Hormone Levels

BN and control participants underwent one day of gastric emptying and appetitive hormone testing at baseline, and BN participants underwent a second day of testing following treatment. The end of treatment study was scheduled during the sixth week of the medication trial (see below).

On the evening before the test day, participants were instructed to eat a standardized dinner that did not include alcohol, no later than 7:00 P.M., and not to eat or drink after 9:00 P.M. Participants reported to the nuclear medicine department at 9:00 AM. An indwelling catheter was placed in a forearm vein for periodic blood sampling. Participants lay in a semi-reclining position with the gamma camera placed directly over the stomach and were asked to consume 600 ml Ensure-Plus (1.5 kcal/g) labeled with 50 μCuries of Technetium-99-DTPA in 5 minutes. This meal has been used in our previous studies of gastric emptying and CCK release, which found significant differences in CCK release between patients with BN and normal controls [4]. Gastric emptying was determined by gamma camera scintigraphy using standard procedures as described previously [4]. Blood samples were be drawn at 20 minutes, 10 minutes, and immediately before food consumption and then at 5 minutes, 10 minutes, 15 minutes and every 15 minutes thereafter until 90 minutes after food consumption. Blood samples were collected in tubes prepared with EDTA and aprotinin (Trasylol) and kept on ice for 2 minutes. The samples were cold centrifuged for 15 minutes, and plasma stored at −80°C.

Plasma CCK, PYY, and ghrelin concentrations were obtained by radioimmunoassay [3]. CCK was analyzed using an RIA kit from ALPCO (standard range 0.4 – 25.0 pmol/L, intra-assay CV = 5.1, interassay CV = 6.1), based on Rehfield [17] that detects the bioactive forms of human CCK, including CCK-58, CCK-32, CCK-22, and CCK-8. Total PYY (1–36 and 3–36) concentrations were measured using an RIA kit from Millipore (standard range 2.6 – 337.5 pmol/L, intra-assay CV = 3.94, interassay CV = 5.89), and total ghrelin (acylated and desacylated) was measured using an assay from Phoenix Pharmaceuticals (standard range 3.0 – 379.0 pmol/L, intra-assay CV = 4.77, interassay CV = 4.53). All hormone assays were performed in duplicate and values were averaged. Preprandial baseline levels of hormones were calculated by averaging the levels obtained at 20 minutes, 10 minutes, and immediately preceding meal consumption. Area under the curve for 0–90 minutes following the meal was determined using the trapezoidal rule. For CCK, in addition to area under the curve, the 15-minute time point was selected for comparison between patients and control participants to capture the presumed peak postprandial response based on previous findings [4].

2.3 Randomized Double-Blind Treatment with Erythromycin or Placebo

Within one week of completing the pre-treatment measures, patients were seen by a psychiatrist at the Eating Disorders Clinic at NYS Psychiatric Institute who initiated treatment with either erythromycin or matching placebo in randomized double-blind fashion. Patients were treated for six weeks. At session #1, patients were instructed to begin erythromycin stearate 250 mg or matching placebo three times a day one half hour before meals. They were instructed by the research psychiatrist to eat three meals per day in order to maximize the effectiveness of the medication on gastric emptying. Patients were seen weekly by the study psychiatrist for brief medication management sessions to assess clinical state, medication adherence, and adverse events. Dosage could be decreased if the patient reported intolerable side effects to the medication, or could be increased to 500 mg three times a day after a two-week period with no improvement of symptoms. At session #7, following the final assessment, the blind was broken by a non-study clinician and patients were informed of their medication assignment. Patients were then referred to a non-study clinician for further treatment. Following our standard procedures, all patients were asked to keep a diary of the number of daily binge eating and vomiting episodes, which was collected at each clinic visit and used to assess their clinical state.

2.4 Statistical Analyses

All comparisons between groups utilized two-tailed t-tests to compare mean values in BN vs. control groups at baseline (Experiment 1) or post-treatment values in patients assigned to erythromycin vs. placebo (Experiment 2). The SAS Mixed procedure was used to compare CCK release in BN and control groups at the 15-minute time point as part of an overall ANOVA in which all the time points were included and the standard error was based on all observations. All analyses were conducted using SAS version 9.2. Data are presented as mean ± SD in text and tables and as mean ± SE in figures.

3. RESULTS

3.1 Experiment 1: Controlled Study of Meal–Related Gastric Emptying and Appetitive Hormone Levels in Bulimia Nervosa

3.1.1 Participant Characteristics

Demographic and clinical features of BN and control participants are presented in . There were no significant differences between groups in demographic variables. Eating Inventory scores were consistent with previous reports in clinical BN samples [18]. Gastric emptying data were obtained for 32 BN participants and 22 control participants, and appetitive hormone data were obtained for 28 BN participants and 22 control participants.

Table 1

Demographic and Clinical Characteristics of Participants (mean ± SD)

	Bulimia Nervosa (N=32)	Control (N=24)	Significance
Age (yrs.)	24.0 ± 3.0	26.1 ± 5.9	NS
Height (in.)	64. 9 ± 2.4	64.7 ± 2.7	NS
Weight (lbs.)	134.4 ± 17.2	135.4 ± 14.2	NS
BMI (kg/m2)	22.4 ± 2.4	22.8 ± 2.2	NS
Ethnicity (number/percent)
• Caucasian	23 (71. 9%)	18 (75.0%)	NS
• Latina	2 (6.3%)	1 (4.2%)
• Black	1 (3.1%)	0 (0.0%)
• Asian	2 (6.3%)	4 (16.7%)
• Mixed/Other	4 (12. 5%)	1 (4.2%)
BDI Score	12.9 ± 8.0
EI Restraint Score	12.8 ± 4.2
EI Hunger Score	8. 3 ± 3.8
EI Disinhibition Score	12.8 ± 2.0
Binge Frequency (episodes/week)	6.2 ± 2.1
Vomit Frequency (episodes/week)	6. 3 ± 2.1

3.1.2 Gastric emptying and appetitive hormone levels

All gastric emptying data and appetitive hormone levels in text are presented as mean value ± standard deviation. There were no significant differences in the slope of gastric emptying between BN and control groups measured in percent remaining per minute (−0.24 ± 0.14 vs. −0.27 ± 0.12 respectively, difference = 0.034 ± 0.132). This corresponds to 21.6 ± 12.6% vs. 24.3 ± 10.8% emptied over 90 minutes in the two groups. There were no significant differences between BN and control groups in mean preprandial cholecystokinin level (0.60 ± 0.41 pmol/L vs. 0.45 ± 0.17 pmol/L, respectively) or postprandial CCK release measured as area under the curve (213.7 ± 156.1 pmol•min/L vs. 201.7 ± 140.0 pmol•min/L, respectively). However, at 15 minutes, mean CCK level in the BN group tended to be lower than that in the control group (3. 86 ± 4.02 pmol/L vs. 5.11 ± 5.26, p=0.1) (see ). There were no significant differences in preprandial PYY level (115.5 ± 87.0 pmol/L vs. 103.1 ± 51.0 pmol/L in BN and control groups, respectively) or in postprandial PYY area under the curve (1559.5 ± 2906.2 pmol•min/L vs. 1776.2 ± 3180.4 pmol•min/L in BN and control groups, respectively). There were no significant differences in preprandial ghrelin level (387.1 ± 185.1 pmol/L vs. 389.0 ± 205.3 pmol/L in BN and control groups, respectively) or in postprandial ghrelin area under the curve (−10211.8 ± 7065.6 pmol•min/L vs. −12001.4 ± 9489.6 pmol•min/L in BN and control groups, respectively) (see ).

Mean (± S.E.) plasma concentrations of CCK (1a), PYY (1b), and ghrelin (1c) in BN vs. control groups prior to and following test meal given from 0–5 minutes.

3.2 Experiment 2: Placebo-Controlled Study of Gastric Emptying, Appetitive Hormone Levels, and Clinical Response in Bulimia Nervosa Following Treatment with Erythromycin

3.

2.1 Participant Characteristics

The study was conducted during the period August 2005 through May 2009. During this period, 250 potential participants were screened by telephone, and 160 of these were determined to be eligible for further screening and were invited to participate in this and, in some cases, additional studies. Forty-four patients were screened in person. Of these, 6 were determined to be ineligible, 3 were determined to be in need of immediate treatment due to severity of illness, and 3 withdrew. Thirty-two patients underwent baseline biological testing and 29 of these returned for randomization to treatment. Fifteen patients were assigned to treatment with erythromycin and 14 were assigned to placebo. Patients who were assigned to treatment with erythromycin did not differ from those assigned to placebo in the demographic or clinical features presented in . Of those who began treatment, 13 patients in each group completed clinical treatment. Ten participants in each group completed post-treatment testing and had gastric emptying and blood sampling for hormone analyses.

3.2.2 Gastric emptying and appetitive hormone levels

The post-treatment slope of gastric emptying in participants who had received erythromycin, measured in percent remaining per minute, was greater than that in participants randomized to receive placebo (−0.339± 0.14 vs. −0.177 ± 0.122, respectively, difference = 0.162 ± 0.131, p=.013), indicating that treatment with erythromycin was associated with more rapid gastric emptying. This corresponds to 30.5 ± 12.6% vs. 16.0 ± 11.0% emptied over 90 minutes in the erythromycin and placebo groups respectively, a difference of 87 grams between pre- and post-treatment assessments. There were no significant differences between erythromycin and placebo groups in post-treatment preprandial levels of CCK (0.43 ± 0.09pmol/L vs. 0.41 ± 0.06 pmol/L) or in postprandial CCK area under the curve (213.9 ± 127.7 pmol•min/L vs. 236.3 ± 107.2 pmol•min/L) (see ). There were no significant differences between erythromycin and placebo groups in post-treatment preprandial PYY level (104. 2 ± 54.1 pmol/L vs. 103.5 ± 35.2 pmol/L) or in postprandial PYY area under the curve 2297.1 ± 2622.2 pmol•min/L vs. 2570.7 ± 3065.0 pmol•min/L) (see ). There were no significant differences between erythromycin and placebo groups in post-treatment preprandial ghrelin level (358.7 ± 142.1 pmol/L vs. 357.0 ± 159.2 pmol/L) or in postprandial area under the curve (−10145 ± 4362.8 pmol min/L vs. −9391.0 ± 6707.6 pmol•min/L) (see ).

Mean (± S.E.) plasma concentrations of CCK (2a), PYY (2b), and ghrelin (2c) at end of treatment in BN patients receiving erythromycin vs. placebo prior to and following test meal given from 0–5 minutes.

3.2.3 Clinical Response

Of 15 patients randomized to receive erythromycin and 14 patients randomized to receive placebo, 13 patients in the erythromycin group and 13 patients in the placebo group completed at least 5 weeks of drug treatment. Of those who completed treatment, 11 patients in the erythromycin group and 12 patients in the placebo group had their dosage increased to the higher level (500 mg. three times daily). Of the 2 patients in the erythromycin group who did not complete treatment, 1 was withdrawn for clinical worsening and 1 withdrew due to lack of improvement. The patient in the placebo group who did not complete treatment was withdrawn due to clinical worsening. No patients had dosage reduced or medication discontinued due to side effects.

There were no differences between treatment groups in baseline or post-treatment binge/vomit frequency calculated as the mean of frequencies at week 5 and week 6. Patients randomized to treatment with erythromycin had weekly binge/vomit frequencies of 9.9 ± 8.7 binge episodes/10.4 ± 8.7 vomit episodes prior to treatment and 11.4 ± 10.7 binge episodes/11.3 ± 10.9 vomit episodes following treatment. Patients randomized to treatment with placebo had weekly binge/vomit frequencies of 8.2 ± 5.4 binge episodes/9.5 ± 6.5 vomit episodes prior to treatment and 7.2 ± 4.1 binge episodes/7.6 ± 4.4 vomit episodes following treatment.

4.

DISCUSSION

The major finding of this study was that treating patients with BN using the motilin agonist erythromycin did not reduce binge eating or vomiting, although it did modestly increase the rate of gastric emptying following a food load from 16% to 30.5% emptied in 90 minutes. In addition, while there were suggestions of baseline abnormalities in gastric emptying and postprandial cholecystokinin release in patients with bulimia nervosa, we did not fully replicate our previous findings. We also did not observe abnormalities in baseline or postprandial levels of PYY or ghrelin in patients with BN.

The finding that BN patients treated with erythromycin did have significantly more rapid gastric emptying than those receiving placebo suggests that the experimental manipulation provided a valid test of the hypothesis that modestly increasing gastric empting would be associated with clinical improvement. However, one explanation for the lack of predicted clinical improvement is that the magnitude of the change in rate of gastric emptying may have been insufficient to impact gastric distension to a degree that would meaningfully affect subsequent meal-related sensations or eating behavior [19]. It is possible that an intervention that more markedly increased the rate of gastric emptying or that more directly influenced postprandial levels of CCK [20,21] or other satiety-related hormones may have been more clinically effective. For example, the two cited studies suggest that the combination of CCK-8 infusion with gastric distension is much more effective than either factor alone in reducing subsequent intake. Thus, it is possible that our previously hypothesized model, in which a reduced rate of gastric emptying and/or abnormal postprandial release of satiety-related hormones are necessary for the perpetuation of the binge-vomit cycle, is applicable only when alterations in gastric emptying or satiety-related hormone release are sufficient to produce large changes in gastric distension.

An alternative explanation is that, in contrast with our previous model, alterations in gastrointestinal physiology, such as reduced rate of gastric emptying or abnormal postprandial hormone release, are not necessary causal factors in the mechanism that perpetuates binge-vomit behavior in patients with BN. This may be the case if alterations in gastrointestinal physiology do not lead to abnormal intrameal satiation or if abnormal satiation does not drive binge-vomit behavior. With regard to the former, a recent study of meal-related perceptions found that, when asked to rate fullness during the course of a large fixed-size (975 gram) meal, patients with BN did not differ significantly from matched controls [22]. This result suggested that the disturbance of intrameal satiation reported in earlier studies [1] may have been related to factors other than disturbed gastrointestinal physiology, such as the individual’s intentions and emotional state, or perceptions of meal size or amount remaining to be consumed. However, the difference between the two studies may also reflect that fact that the size of the meal in the study of Zimmerli et al. [22] was considerably smaller than the typical size of ad lib binge episodes in the earlier study [1], and it is conceivable that disturbances in gastrointestinal physiology occur only when the volume of gastric contents exceeds a relatively high threshold.

The study also attempted to replicate previous findings regarding baseline and postprandial levels of appetitive hormones in individuals with BN. A recent review and meta-analysis of studies of baseline and postprandial levels of appetitive hormones in individuals with eating disorders found that studies were relatively few in number, particularly if limited to those including patients with BN, and findings were heterogeneous [2]. However, variability in the size and composition of the food stimulus may contribute to variability in findings. With regard to studies of BN, there is no clear consensus regarding baseline or postprandial levels of CCK, PYY, or ghrelin. Two studies [11,12] reported diminished PYY response to a meal, and three studies [4,23,24] reported marginally or significantly diminished CCK postprandial response, with two studies [25,26] failing to find this. Our current findings therefore add marginal support to earlier findings of diminished postprandial CCK response, at least at the 15-minute postprandial time point, the presumed peak response point.

There are several additional limitations that must be taken into account in interpreting the findings, and that limit the generalization of these results. First, regarding our CCK assays, we employed a radioimmunoassay, rather than the bioassay used in our previous study [4]; however, the radioimmunoassay detects the bioactive forms of CCK and thus produces results comparable to a bioassay [27,28]. It is also possible that aspects of stomach functioning other than emptying rate, such as gastric relaxation following food consumption [5] or sensitivity to gastric distension [18] may play a more direct causal role. As we did not study these aspects of gastric functioning in the current study, we could not assess the effect of erythromycin treatment on them and cannot rule out the possibility that their normalization for a more sustained period might be associated with clinical improvement. Additionally, although vomiting was the predominant method of purging for all patients, we did not systematically assess the occasional use of other methods of purging that may have contributed to abnormal gastrointestinal function or may have responded differently to erythromycin treatment. Finally, since our treatment used medication and medical management only, it is possible that normalizing gastric emptying may be of adjunctive benefit but is not helpful as a sole intervention. Future studies may benefit from the inclusion of additional outcome measures including food intake or level of exercise in response to drug treatment, changes in weight or body composition, and changes in mood or in the subjective experience of eating.

4.1 Conclusions

In sum, with the quantitative limitations noted above, the current study fails to support a role for erythromycin in the treatment of BN. While these results are consistent with the inference that the abnormal intrameal satiation previously observed when individuals with BN binge eat does not result solely from delayed gastric emptying, more quantitative studies of the effect of prokinetic agents are needed, as erythromycin affected gastric emptying only modestly in this study. Moreover, interventions that directly impact CCK release or release of other satiety-inducing hormones might prove a more effective therapeutic approach. Further studies are needed to clarify the role of previously observed abnormalities in gastric functioning in the causal chain leading to binge eating and vomiting, and to better understand the interaction of cognitive and biological factors in initiating and/or maintaining these behaviors.

​

Highlights

• We examine gastric emptying and post-meal gastrointestinal hormone release in bulimia nervosa.

• Gastric emptying is normal and early post-meal CCK release marginally low in bulimia nervosa.

• Erythromycin treatment of bulimia nervosa produces a modestly increased gastric emptying rate.

• Erythromycin treatment of bulimia nervosa is not associated with clinical improvement.

Acknowledgments

This work was supported by NIMH grant MH-42206, NIH grants DK-68392 and DK-74046, and the New York Obesity Research Center NIH grant DK-26687. We would like to thank Alexia Spanos for her contributions to this study.

Footnotes

Publisher’s Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

References

1. Kissileff HR, Wentzlaff TH, Guss JL, Walsh BT, Devlin MJ, Thornton JC. A direct measure of satiety disturbance in patients with bulimia nervosa. Physiol Behav. 1996;60:1077–85. [PubMed] [Google Scholar]2. Prince AC, Brooks SJ, Stahl D, Treasure J. Systematic review and meta-analysis of the baseline concentrations and physiologic responses of gut hormones to food in eating disorders. Am J Clin Nutr. 2009;89:755–65. [PubMed] [Google Scholar]3. Geliebter A, Melton PM, McCray RS, Gallagher DR, Gage D, Hashim SA. Gastric capacity, gastric emptying, and test-meal intake in normal and bulimic women. Am J Clin Nutr. 1992;56:656–61. [PubMed] [Google Scholar]4. Devlin MJ, Walsh BT, Guss JO, Kissileff HR, Liddle RA, Petkova E. Postprandial cholecystokinin release and gastric emptying in patients with bulimia nervosa. Am J Clin Nutr. 1997;56:114–20. [PubMed] [Google Scholar]5. Walsh BT, Zimmerli E, Devlin MJ, Guss J, Kissileff HR. A disturbance of gastric function in bulimia nervosa. Biol Psychiatry. 2003;54:929–33. [PubMed] [Google Scholar]6. Geliebter A, Hashim SA. Gastric capacity in normal, obese, and bulimic women. Physiol Behav. 2001;74:743–6. [PubMed] [Google Scholar]7. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4. Washington, DC: American Psychiatric Association; 2000. pp. 589–94. (Text Revision) [Google Scholar]8. Szmukler GI, Young GP, Miller G, Lichtenstein M, Binns DS. A controlled trial of cisapride in anorexia nervosa. Int J Eat Disord. 1995;17:347–57. [PubMed] [Google Scholar]9. Gumaste V, Baum J. Treatment of gastroparesis: an update. Digestion. 2008:173–9. [PubMed] [Google Scholar]10. Wysowski DK, Corken A, Gallo-Torres H, Talarico L, Rodriguez EM. Postmarketing reports of QT prolongation and ventricular arrhythmia in association with cisapride and Food and Drug Administration regulatory actions. Am J Gastroenterol. 2001;96:1698–703. [PubMed] [Google Scholar]11. Kojima S, Nakahara T, Nagai N, Muranaga T, Tanaka M, Yasuhara D, Masuda A, Date Y, Ueno H, Nakazato M, Naruo T. Altered ghrelin and peptide YY responses to meals in bulimia nervosa. Clin Endocrinol (Oxf) 2005;62:74–8. [PubMed] [Google Scholar]12. Monteleone P, Martiadis V, Rigamonti AE, Fabrazzo M, Giordani C, Muller EE, Maj M. Investigation of peptide YY and ghrelin responses to a test meal in bulimia nervosa. Biol Psychiatry. 2005;57:926–31. [PubMed] [Google Scholar]13. Fairburn CG, Cooper Z. The Eating Disorder Examination. In: Fairburn CG, Wilson GT, editors. Binge eating: nature, assessment, and treatment. 12. New York: The Guilford Press; 1993. pp. 317–60. [Google Scholar]14. First MB, Spitzer RL, Gibbon M, Williams JBW. Structured clinical interview for DSM-IV axis I disorders (SCID) New York: New York State Psychiatric Institute, Biometrics Research; 1995. [Google Scholar]15. Beck AT, Ward CH, Mendelson M, Mock J, Erbaugh J. An inventory for measuring depression. Arch Gen Psychiatry. 1961;4:561–71. [PubMed] [Google Scholar]16. Stunkard AJ, Messick S. The three-factor eating questionnaire to measure dietary restraint, disinhibition and hunger. J Psychosom Res. 1985;29:71–83. [PubMed] [Google Scholar]17. Rehfield JF. How to measure cholecystokinin in tissue, plasma and cerebrospinal fluid. Regul Pept. 1998;78:31–9. [PubMed] [Google Scholar]18. Zimmerli EJ, Walsh BT, Guss JL, Devlin MJ, Kissileff HR. Gastric compliance in bulimia nervosa. Physiol Behav. 2006;87:441–6. [PubMed] [Google Scholar]19. Geliebter A. Gastric distension and gastric capacity in relation to food intake in humans. Physiol Behav. 1988;44:685–8. [PubMed] [Google Scholar]20. Muurahainen N, Kissileff HR, Derogatis AJ, Pi-Sunyer FX. Effects of cholecystokinin-octapeptide (CCK-8) on food intake and gastric emptying in man. Physiol Behav. 1988;44:645–9. [PubMed] [Google Scholar]21. Kissileff HR, Carretta JC, Geliebter A, Pi-Sunyer FX. Cholecystokinin and stomach distension combine to reduce food intake in humans. Am J Physiol Regul Integr Comp Physiol. 2003;285:R992–8. [PubMed] [Google Scholar]23. Geracioti TD, Liddle RA. Impaired cholecystokinin secretion in bulimia nervosa. N Engl J Med. 1988;319:683–8. [PubMed] [Google Scholar]24. Keel PK, Wolfe BE, Liddle Ra, De Young KP, Jimerson DC. Clinical features and physiological response to a test meal in purging disorder and bulimia nervosa. Arch Gen Psychiatry. 2007;64:1058–66. [PubMed] [Google Scholar]25. Phillip E, Pirke KM, Kellner MB, Krieg JC. Disturbed cholecystokinin secretion in patients with eating disorders. Life Sci. 1991;48:2443–50. [PubMed] [Google Scholar]26. Fujimoto S, Inui A, Kiyota N, Seki W, Koide K, Takamiya S, Uemoto M, Nakajima Y, Baba S, Kasuga M. Increased cholecystokinin and pancreatic polypeptide responses to a fat-rich meal in patients with restrictive but not bulimic anorexia nervosa. Biol Psychiatry. 1997;41:1068–70. [PubMed] [Google Scholar]27. Hoecker M, Schmidt WE, Cruetzfeldt W, Choudhury AR, Nustede R, Schafmayer A, Foelsch UR. Determination of plasma cholecystokinin (CCK) concentrations by bioassay and radioimmunoassay in man. A critical evaluation. Regul Pept. 1992;37:255–69. [PubMed] [Google Scholar]28. Hoecker M, Schmidt WE, Wilms HM, Lenhoff F, Nustede R, Schafmayer A, Foelsch UR. Measurment of tissue cholecystokinin (CCK) concentrations by bioassay and specific radioimmunoassay: characteristics of the bioactivity of CCK-58 before and afer tryptic cleavage. Eur J Clin Invest. 1990;20 (Suppl 1):S45–S50. [PubMed] [Google Scholar]

Gastroparesis | Gastrointestinal Society

Click here to download a PDF of this information.

The term ‘gastro’ refers to the stomach, and ‘paresis’ means partial paralysis; therefore, gastroparesis means partial paralysis of the stomach. To understand what goes wrong in gastroparesis, it is important to know how a healthy digestive tract functions. When we eat, we start by chewing and swallowing (ingesting), which requires conscious effort. Once the food reaches the esophagus, an automatic, rhythmic motion (peristalsis) takes over, propelling the contents all the way through the digestive tract. Typically, the passage of food from one area of the digestive tract to the next is precisely coordinated, so that food stays in each area for just the right amount of time. For the stomach, this is approximately two hours.

However, in those with gastroparesis, the food does not move from the stomach into the intestine as quickly as it should (delayed gastric emptying). Gastroparesis is a motility disorder, which means there is no physical obstruction preventing timely digestion, but rather a problem with muscular activity regulation. It occurs when the pair of nerves that connects the brainstem to the gastrointestinal tract (vagus nerve) is damaged or not functioning properly. Since the vagus nerve is unable to send the necessary messages to ensure that the muscles in the stomach continue to work normally, food remains in the stomach for too long, leading to symptoms.

Causes of Gastroparesis

The most common cause of gastroparesis is diabetes mellitus type 1 or type 2. High levels of glucose in the blood can cause chemical changes to the vagus nerve. This type of gastroparesis can be especially dangerous, because the delayed gastric emptying leads to more intense blood sugar spikes in those with diabetes, causing a cycle of blood sugar highs and lows that continues to affect the vagus nerve.

Gastroparesis is typically associated with some form of damage to the vagus nerve, which can occur in a range of situations, including from various mineral deficiencies, eating disorders, opioid medications, certain antidepressants, and surgeries in the upper gastrointestinal tract, such as gastrectomy or bariatric surgery. Other causes of gastroparesis, although very rare, include connective tissue diseases such as scleroderma and Ehlers-Danlos syndrome, and neurological conditions such as Parkinson’s disease. In about a third of cases, the cause of gastroparesis is unknown (idiopathic). In some cases, such as those caused by certain medications or eating disorders, the gastroparesis can be temporary, with normal digestive function returning upon medication adjustment or adapting to healthy eating habits.

Prevalence of Gastroparesis

Gastroparesis affects approximately 4% of the population and is more common in women. Many people with gastroparesis also have diabetes, and 50% of those affected had diabetes before the onset of their gastroparesis.

Gastroparesis Symptoms & Complications

The most common symptoms of gastroparesis include feeling full from small amounts of food, nausea, vomiting, reduced appetite, abdominal pain, heartburn or gastroesophageal reflux disease (GERD), and regurgitation. These symptoms can lead to weight loss and nutrient deficiencies. Other symptoms include bloating, muscle weakness, and night sweats. Since the digestive system doesn’t work smoothly, those with the condition also experience periods of low blood sugar while the food remains in the stomach, and high blood sugar when it eventually reaches the intestines.

Sometimes, more severe complications can occur due to delayed gastric emptying. Individuals can experience obstructions caused by masses of solid hardened food (bezoars). Often, bezoars will pass on their own, but other times they require treatment in the form of oral solutions to help dissolve them or, in severe cases, surgery.

If excessive vomiting is a symptom, it can cause its own set of complications, including dehydration and malnutrition. In those who have diabetes and gastroparesis, controlling blood sugar can become very difficult due to the irregular release of food into the small intestine.

Diagnosing Gastroparesis

Your physician will review your symptoms and medical history and complete a physical examination, including blood tests. If he or she finds it likely that you have gastroparesis or is unsure and wants to rule out other diseases and disorders, there are a few tests available. This is especially important with gastroparesis, because many of the symptoms are similar to other disorders, such as functional dyspepsia.

Gastric emptying scans allow your healthcare team to measure the speed at which you digest food. For this test, you consume a tiny amount of radioactive material with a small meal, which allows technicians to monitor the rate at which it passes through your digestive system by periodically using a camera to check where the radioactive meal is. If it stays in the stomach for too long, then it can indicate gastroparesis.

An upper gastrointestinal series involves consuming a barium drink in front of an x-ray machine after fasting. The barium is a chalky liquid that shows up on x-rays, allowing the technicians to see details in the gastrointestinal tract. This can help them find any anomalies in stomach function.

Gastroscopy involves a physician using a small, flexible tube with a camera and a light (endoscope) to look at the upper parts of the digestive system, including the esophagus, stomach, and duodenum. This test is helpful to detect bezoars or any other abnormalities in the stomach.

Abdominal ultrasound is useful for identifying if there are any physical abnormalities that might be causing symptoms.

Gastric or duodenal manometry involves using a long thin tube that measures muscle strength and patterns within the esophagus and through the lower esophageal sphincter into the stomach.

Management of Gastroparesis

The management of gastroparesis can include simple dietary changes, medications, and even surgery depending on the disease severity.

Lifestyle and Dietary Changes

In individuals with mild gastroparesis, a few changes to dietary habits can largely reduce symptoms. Most of these changes focus on reducing the amount of food you eat at once, because overeating makes it even more difficult for your stomach to empty. Consuming smaller meals more frequently, rather than two or three large meals, can help. You may also find relief by eating mostly soft or liquid foods, such as soups and smoothies. Chewing each bite very well and consuming non-fizzy liquids with meals can also make digestion easier. Avoiding or limiting high fibre and high fat foods can reduce discomfort, since these foods typically take longer to digest. For some individuals, supplemental nutrition beverages can help ensure adequate nutrient intake.

If you have diabetes, make sure to keep glucose tablets or hard candies on hand. You can use them to raise your blood sugar, because they are easily absorbed, if gastroparesis is causing low blood sugar. A registered dietitian can offer advice if you are unsure what to eat so that you meet your nutrition requirements when you have gastroparesis.

Medications

The medications available for gastroparesis don’t treat the underlying disease, but they help to alleviate symptoms. There are two primary medication types available:

Motility agents increase the speed of peristalsis, causing the stomach to empty more quickly, and include metoclopramide (Reglan®, Maxeran®) and domperidone (Motilium®). NOTE: Health Canada pulled a gastroprokinetic agent, cisapride, from the market at the turn of the century due to serious health concerns and deaths. However, some physicians still cautiously prescribe cisapride, which increases motility in the upper gastrointestinal tract, for severe cases of gastroparesis. Compounding pharmacies can acquire the drug under special circumstance.

Antiemetics reduce nausea and vomiting, and include medicines such as prochlorperazine and promethazine.

Surgery

For those who are unable to get symptoms under control through dietary changes and medications, there are a few surgical options that may offer relief.

A gastric electric stimulator is an implanted device that uses mild, controlled electrical pulses to stimulate the smooth muscles in the digestive tract and speed up gastric emptying. However, this treatment does not work for everyone, and is not available in all areas.

Botox (botulism toxin) injected in the sphincter that connects the stomach to the small intestine (pylorus) can help relax the sphincter so that it more easily allows food passage into the small intestine. Botox injections don’t work for everyone, they are only a temporary solution, and can become less effective in subsequent injections.

A feeding tube surgically attached at the entry to the small intestine can offer a last resort for those who are completely unable to take nutrients into the stomach in either solid or liquid form.

Gastroparesis Outlook

Gastroparesis is typically a chronic condition with potentially dangerous side effects. For some individuals, being more careful about the frequency and types of foods they consume is enough to live a relatively normal life, but for others, ongoing medications and even surgery might be necessary. Quality of life is often diminished with gastroparesis. Those who have both diabetes and gastroparesis need to be especially diligent.

Want to Learn More?

Image Credits (top to bottom): © bigstockphoto.com/Ammentorp, © bigstockphoto.com/designua

Can We Treat Eating Disorders and Gastroparesis Together?

Many eating disorder treatment programs emphasize the sentiment that “food is medicine.”

“Nutrition will restore weight that needs to be restored.”

“Nutrition will fix medical complications.”

“Nutrition will help to maintain your set point theory weight.”

“Nutrition will help your mood disorders and obsessive thoughts to decrease.”

“Eating is the best way to fight the eating disorder.”

Even putting up quotes like, “The best way to fight the eating disorder is to pick up the fork and rebel.”

I find these quotes to be inspiring, choice-based, and recovery minded. I am an advocate for quotes like these to be put up in treatment programs, recovering individual’s rooms, houses, etc.

But, what happens when a chronic illness or a complication of the eating disorder makes it so that the individual cannot take their “medicine?” When they can’t eat?

I was diagnosed with gastrointestinal dysmotility (gastroparesis) after years of restricting, purging, and abusing laxatives. It is a common and can be life-threatening complication of eating disorders. It causes symptoms like nausea, vomiting, severe gastroesophageal reflux disease, regurgitation, bloating, water retention, constipation, diarrhea, early fullness, and so much more. It is hell to live with, and, for many, certain types of foods, eating too frequently, eating certain groups of food, eating a high volume of food, or even eating at all, can cause vomiting, extreme pain, or extreme nausea.

People with dysmotility or gastroparesis have delayed gastric emptying, meaning it takes them hours to days longer to digest a meal than it would for the average person due to a partially (or in some cases, completely) paralyzed digestive track.

How do people who have both an eating disorder and dysmotility balance eating disorder recovery?

At my medically sickest, I could not keep anything down. I wanted to eat more than anything, I wanted to leave the hospital, mentally I wanted to fight off my anorexia, but I couldn’t because of my dysmotility. I would be plagued with bloating after every meal, vomiting occasionally, not going to the bathroom for weeks, and pain so intense I would not leave the bed.

Most eating disorder programs are not equipped to treat people with gastrointestinal illnesses or chronic illnesses, even though they are common complications of eating disorders.

I wonder how we could shift from medical and behavioral stabilization to improvement of quality of life?

I have thought about the idea of treating both gastroparesis and eating disorders together, in the same treatment program. What if we were able to treat both diseases at the same time? How many people would be able to get the treatment they needed and not fall through the cracks of the system?

Since getting to a place where in eating disorder recovery where we do not have fear foods and we are able to intuitively eat is often the goal, where do people with gastroparesis fit in? Many people with gastroparesis do not get hunger cues, and cannot eat certain foods.

My article is just one voice. For many, eating disorder recovery is truly about learning to intuitively eat again. But, for me, as someone who struggles with dysmotility, it is not. For me, recovery is about being able to sit with food inside of me, cope with the physical sensations and pain, and work through the waves and guilt. For me, recovery is about physically keeping food down. Of course, there is so much more to recovery for me than just those few ideas. But, my idea of recovery looks different than many treatment programs for eating disorders ideas of recovery look like.

I wish we could start the discussion about treating gastrointestinal issues like gastroparesis that coexist with eating disorders.

We want to hear your story. Become a Mighty contributor here.

Thinkstock Image By: JNemchinova 

Gastroparesis and bulimia

The article was written by Anna Vladimirovna Nazarenko on the basis of 17 years of practical experience of working with RPP. Anna Vladimirovna specializes in drug-free treatment, within the framework of humanistic psychotherapy, individual counseling, non-stationary treatment of bulimia and anorexia.

Many eating disorder treatment programs emphasize the belief that “Food is the cure.”

“Food will restore weight and restore your life.”

“Food will save you from disease.”

“Food will help reduce your emotional problems and get rid of obsessive thoughts.”

“Food is the best way to fight an eating disorder.”

And especially this one – “The best way to fight an eating disorder is to pick up a fork and heal.”

I find these quotes inspiring for those seeking recovery.I support these thoughts and would like to see similar quotes placed in treatment programs for eating disorder centers.

But what happens when, due to chronic bulimia or anorexia, a person is unable to take their “medicine”? When a person cannot eat? When a person cannot live SATURATION.

Speaking about Gastroparesis , I decided that it would be appropriate to tell a little about how I lived it, how I lived The heaviness in the stomach – it’s Satiety.

My personal history with RPP is long: 2 years of anorexia, 10 years of bulimia and long-term use of antidepressants and tranquilizers.

The result of my adventures with RPP – 20 years ago I was diagnosed with impaired gastrointestinal motility (gastroparesis), – after many years of anorexia and bulimia (10 years of cleansing and laxative abuse). It is a common and life-threatening complication of an eating disorder.It causes symptoms such as nausea, vomiting, severe gastroesophageal reflux disease, regurgitation, bloating, water retention, constipation, diarrhea, premature fullness, and more. This is hell, and the normal relationship with food for healthy people becomes a big problem: eating too often, eating certain food groups, eating too much food, or even eating at all can cause vomiting, severe pain or severe nausea.

People with impaired motility or gastroparesis for a long time cannot empty the stomach, which means that they take much longer (from several hours to several days) to digest food than for the average person, due to the partially paralyzed digestive tract.

How do people with eating disorders and motor impairments reconcile recovering from an eating disorder and living gastroparesis?

At the most painful moment from a medical point of view, I could not digest anything – I could not be SATED – I could not panic. It was not only the fear of calories, fear of gaining weight, but also the terrifying, maddening SATURATION (another mystical version of my psychotherapist, that the reason for this physical state: “I cannot accept my father” – crashed against all the physical processes in the gastrointestinal tract) …Now I, being a completely healthy person, able to digest: lamb, cake, butter and any other products, I can call SATURATION, and then I called it HEAVY.

I wanted to eat more than anything else, I wanted to leave another hospital, mentally I wanted to overcome my bulimia, but I could not because of motor impairment. I was tormented by bloating after every meal, sometimes vomiting; I didn’t go to the bathroom for several weeks, my stomach was swollen from every meal, and the pain was so bad after most of the meals I couldn’t get out of bed and breathe.Then I thanked another psychotherapist for their help, said that everything was ok, that I was healthy, and went home – again for bulimia and laxatives. And then I felt physically good. It was almost impossible to be well fed. Either baby food or bulimia – that’s the only way I could get rid of gastroparesis. Gastroparesis was the result of my years of RIP, not the cause. I didn’t know what happened to me for many years. Because it was impossible at that time to unite the doctors into one that my Gastroparesis is a consequence of my RPP and that everything should be treated together.Indeed, 20 years ago there was no such specialization as a specialist in the field of RPE.
The psychotherapist had no experience in gastroenterology, dietetics, and the gastroenterologist had no education in Psychology. The circle is complete.

Most eating disorder programs in Europe, the United States and even more so Russia are not designed to treat people with gastrointestinal or chronic diseases, even if they are complications of eating disorders.And if you look at the statistics of our work and the number of clients over 17 years, then almost 98% had all the above described symptoms, someone had more, someone less, but they were, and these problems with the gastrointestinal tract interfered with the therapy of bulimia and anorexia with classical psychotherapy or independent attempts to recover at home.

And this is one of the most difficult problems on the road to recovery from RPF. Combine the treatment of Gastroporesis with the recovery from bulimia and anorexia. We often write that antidepressants do not help in therapy because they do not work with the gastrointestinal tract, do not create eating habits consciously, do not teach to understand food and listen to the work of your stomach: which food is right for you and which is not, and with what food still has to train.Yes, for 1 or 2 months, antidepressants can help: calm down, sleep, that is, relieve tension caused by prolonged hunger, fear of food and obsessive thoughts about food, but when issues with SATURATION are not resolved, she is not accustomed, a new eating habit is not created , the relationship with food is not established, then after a while the RPP returns again. But statistics can arise in this way. The patient received antidepressants, the breakdowns were gone, the psychotherapist was happy, Fluoxetine, aka Prozac, too, the client happily thanked him and left.But you need to start eating and eating in an adult way, alone, in your apartment, seriously, eating with gusto: main courses, “scary” soups too, and also birthdays, weddings and funerals, restaurants and pizza. And SATURATION is unbearable. Then everything is new.

For many, it takes a couple of months to restore the work of the gastrointestinal tract, for some for six months, and for others for years. It all depends on the type and duration of the disease, as well as the personal characteristics of the patient.

I thought that treating gastroparesis and eating disorders together, in the same treatment program, would be the best solution.Treat both diseases at the same time. This practice in my therapy helps most people get the treatment they need for ADR and not fall out of order when Satiety appears.

For many, recovering from an eating disorder really means learning to eat freely again. But for me, as someone who fought on my own 20 years ago with motor impairment, this is not entirely true. For me, recovery is an opportunity to sit quietly with food in my stomach, cope with uncomfortable physical sensations, pain in the gastrointestinal tract, go through waves of anxiety and guilt, and forget about these feelings at the table.For me, convalescence is a physical calm experience of Satiety. My view of recovery is different from many eating disorder treatment programs.

It takes a little longer to treat Bulimia with gastroparesis, but it can be cured with a little patience, but these expended forces will definitely pay off, because at the end of your work you will get a calm stomach, comfort from satiety, emotional and conscious freedom from food, get off sugar needle and get for all this health and a slim or thin body (as you like :))

If you need support, call +7 (903) 098-77-55 (WhatsApp) or email info @ bulimii.net. RARPP specialists will help you cope with bulimia and you can start a new life without an eating disorder as soon as possible.

information on the site is not a public offer

Consequences of bulimia – the most common diseases

Bulimia nervosa is a mental disorder characterized by increased appetite, a desire to overeat and the development of a depressive complex against the background of the consequences of an excess diet.

Bulimia is a progressive and paroxysmal disorder, at such moments a person is not aware of either the amount of food taken or the variety of the menu. Over time, the frequency of seizures increases, which contributes to the excess accumulation of fatty deposits in the subcutaneous tissue. An increase in body weight and a violation of the physiological forms of the body leads to the development of emotional experiences with a further transition to an anxiety state and depressive disorder. In an attempt to lose extra pounds, against the background of active emotional experiences, the patient begins to seek various, sometimes not the most humane, ways to remove the food eaten.

Artificial induction of the gag reflex, massive use of laxatives and diuretics, heavy physical activity and exhausting fasting, leading to the development of anorexia – a classic set of actions widely used by all bulimics. Unfortunately, such a choice in the fight against the disease does not lead to any positive results, the situation is only getting worse. The attachment to overeating is so great that, in spite of any complications, at the moments of an attack, the patient continues to absorb food, and then, repenting, again resorts to savage methods of removing it.In advanced cases, such methods of excretion of food can be counted several times during the day, which leads to exhaustion. However, losing weight does not stop the patient, who continues to believe that every spoonful of food swallowed is harmful to him.

In the absence of timely and correct assistance, there are frequent cases of death, either due to suicide, due to a deep depression, or biological weakening of vital systems and organs against the background of prolonged anorexia, most often due to cardiac arrest.

During the course of the disease, due to independent and uncontrolled attempts to “cleanse”, many associated pathological changes develop, which often acquire sufficient severity, complicating the genesis of bulimia and its treatment.

Gastroesophageal reflux disease and esophageal pathology

GERD is a severe chronic disease characterized by long-term treatment and frequent relapses. Chronic gastric reflux is a disease in which there is a reverse, uncontrolled release of the contents of the stomach or duodenum into the lumen of the lower esophagus.

Clinically, GERD is manifested by chronic heartburn and frequent sour belching against a background of sharp severe pain in the stomach, passing into the chest region, neck and left side of the chest.

The manifestation of reflux is facilitated by many factors, the main of which are overeating, a constant full stomach, a decrease in the contractility of the esophagus. The disease is characterized by a certain vicious circle – the damaged sphincter between the stomach and the esophagus is in a loosely closed state, which contributes to the return of acidic contents into the esophagus, the mucous membrane of which is irritated, causing additional harm to the sphincter.

The etiological factor of reflux in bulimia nervosa is based on constant overflow of the stomach due to overeating and stimulation of an artificial gag reflex.

Esophagitis is an inflammatory disease of the esophageal mucosa, which is a companion of reflux, which complements the overall clinical picture with a constant sensation of a lump in the throat, painful swallowing and progress of a food coma, nausea and persistent vomiting.

It is extremely rare that spontaneous rupture of the esophagus occurs when its contents fills the free lumens of the chest cavity, which is accompanied by severe pain and leads to a sudden death.The reason for the rupture of the esophagus is the thinning of its walls, due to chronic inflammatory reactions, which are subjected to strong pressure at the time of the vomiting reflex and they, not withstanding the load, burst.

Dehydration of the body

Frequent vomiting and diarrhea lead to a violation of the flow of water into the body, which leads to its general deficiency – dehydration, or dehydration. Severe painful sensations begin to manifest themselves already with a general lack of water in 10%, with a decrease in the level of losses to 20% – a fatal outcome occurs.

Chronic bulimia, especially in the late stages of anorexia, is always accompanied by dehydration, which is characterized by general weakness, increased drowsiness, rapid physical fatigue, dizziness, nausea, headaches and discomfort in the heart, as well as dry skin.

Hypokalemia

The pathological condition in hypokalemia is characterized by an acute shortage of potassium in the body – the most important trace element involved in many physiologically important body processes.

Significant losses of potassium, in bulimia nervosa, occur due to its abundant excretion in the urine and diarrhea, as well as in case of insufficient intake from food.

When the level of potassium ions in the blood drops below 3 mmol / l, symptoms of fatigue, muscle weakness, and night cramps, characterized by severe pain, begin to appear. With prolonged potassium deficiency, temporary paralysis or paresis, shortness of breath, and chronic constipation may occur.

With the uncontrolled use of diuretics and laxatives, in 98% of cases, a water-electrolyte imbalance occurs, which is characterized not only by a deficiency of water and potassium, but also by other vital microelements that regulate metabolism in the cells of the body.The chronic course of disturbances in water and electrolyte metabolism often ends with the manifestation of serious disturbances in the work of the heart and ends in death, which is one of the main reasons for the high mortality rate among patients with bulimia nervosa.

Injuries to the oral cavity, pharynx and larynx

Very often, when examining the oral cavity in patients with bulimia nervosa, numerous injuries to the mucous membrane of the oral cavity, pharynx and larynx are found, due to mechanical damage to the fingers and nails during artificial induction of the gag reflex.Injuries, as a rule, are of a chronic inflammatory nature, which is complicated by the constant exposure of the wounds to the acidity of the vomit and a low level of saliva secretion, which has disinfecting properties that accelerate the healing of injuries in the oral cavity.

Gastroparesis

The term gastroparesis is a digestive disorder, which is characterized by a decrease in the muscle tone of the stomach walls and, as a result, its rapid overflow even with a small amount of food eaten.

Normally, the walls of an empty stomach are in a constricted static state. With the first portions of food, the walls of the stomach begin to stretch, increasing its useful space, secretions of the digestive glands begin to be secreted, acid is produced, peristalsis is triggered, which ensures further advancement of the food coma, partially treated with pepsin and hydrochloric acid, further – for digestion into the small intestine.

With gastroparesis, this complex of digestive processes starts very sluggishly or does not start at all for a long time.With each sip of food, there is a rapid overflow of an unprepared stomach and, as a result, rejection in the form of a gag reflex – the protective functions of the digestive system are triggered, which mistakenly consider food to be a toxic, foreign environment.

Gastroparesis is often caused by overloading of the smooth muscles of the gastric walls, due to regular calls to the gag reflex among patients with bulimia nervosa.

Mallory-Weiss Syndrome

The disease is sometimes called Mallory-Weiss tears.The pathology is characterized by superficial cracks and ruptures of the upper layers of the mucous membrane of the abdominal esophagus and the cardiac part of the stomach, due to regular vomiting in a crowded stomach. A very common pathology in bulimia nervosa.

Cracks have a characteristic shape that resembles a flowing tear, which is why the disease was given the appropriate name.

Clinically, the disease is characterized by soreness in the epigastrium, behind the breastbone, frequent urge to vomit, vomit often contains lumps of bloody mucus and black, coagulated blood.

Stomach ulcer

In acute digestive disorders caused by frequent overeating and the subsequent process of vomiting, favorable conditions are often created for the development of peptic ulcer and duodenal ulcer.

Even during physiologically normal digestion, the gastric mucosa always experiences serious stress due to mechanical pressure from food volumes, irritation with small particles of indigestible particles, high concentration of gastric acid and the reactivity of pepsin, a digestive enzyme produced in the stomach.A healthy digestive system has a number of protective and adaptive functions that provide a favorable restoration of the mucous membrane with minor damage.

With bulimia nervosa, patients, trying to cleanse the stomach again, do not think at all about the possible consequences of digestive disorders, which in 99% of cases manifest themselves in the form of a peptic ulcer.

Digestive juices, which were allocated to digest the volume of newly received food, begin to actively destroy the mucus and mucous membrane of the stomach, due to the lack of food after artificially induced vomiting.Thus, the most important protective factor is damaged, which ultimately leads to deep damage to the mucous epithelium and underlying layers.

In the formed pathological foci, pathological microorganisms Heliobacter begin to accumulate, one of the few representatives capable of surviving and actively multiplying in the silno acid environment of the stomach.

The activity of microorganisms, an acidic environment and constant trauma by contents and vomiting, creates conditions for the active development of an ulcerative focus, which, without the use of timely and correct treatment, will end with a through perforation of the stomach wall and the spread of gastric contents in the abdominal cavity.This phenomenon will cause unbearable pain and sudden death of the patient, usually within a very short time, depending on the diameter of the perforation.

Pathology of teeth and salivary glands

Frequent emetic processes ensure constant contact of the oral cavity with the acidic environment of the stomach contents, which, with regular exposure, causes damage to the enamel, and then to the dentin of the teeth.

This pathological process is called erosion of tooth enamel, or periolysis, characterized by the slow dissolution of tooth enamel in the hydrochloric acid of the stomach.The pathological process, due to its slow course, is not immediately noticeable. First of all, dark spots appear on the enamel of the incisors of the upper jaw and canines, which, over time, increase and merge into one focus. The lesions on the teeth are always symmetrical.

Subsequently, funnel-shaped depressions are formed on the surface of the teeth, active erasure of the surface of the teeth begins, this is especially clearly visible on the lower incisors. If the site of the focus of erosion was preceded by a carious lesion, the complete destruction of the tooth in this place is inevitable.

The constant effect of acidity of gastric contents has a serious pathological effect on the activity of the salivary glands, primarily due to chemical irritation of their excretory lumens. In addition, the acidic environment in the oral cavity promotes active secretion, and with more prolonged exposure, inhibition of saliva production. Such a load ultimately leads to hypertrophy of the salivary glands and a decrease in saliva production – hyposalivation. This effect further aggravates the digestion process and increases the dryness of the oral cavity, contributing to the development of pathological foci in it.

90,000 Gastroparesis or how to learn to be full? | Russian RPP Association

The article was written by Anna Vladimirovna Nazarenko on the basis of 17 years of practical experience with RPP. Anna Vladimirovna specializes in drug-free treatment, within the framework of humanistic psychotherapy, individual counseling, non-stationary treatment of bulimia and anorexia.

Many eating disorder treatment programs emphasize the belief that “Food is the cure.”

“Food will restore weight and restore your life.”

“Food will save you from disease.”

“Food will help reduce your emotional problems and get rid of obsessive thoughts.”

“Food is the best way to fight an eating disorder.”

And especially this one – “The best way to fight an eating disorder is to take a fork and heal.”

I find these quotes inspirational for those seeking recovery. I support these thoughts and would like to see similar quotes placed in treatment programs for eating disorder centers.

But what happens when, due to chronic bulimia or anorexia, a person is unable to take their “medicine”? When a person cannot eat? When a person cannot live SATURATION.

Speaking about Gastroparesis , I decided that it would be appropriate to tell a little about how I lived it, how I lived The heaviness in the stomach – it’s Satiety.

“My personal story from RPP is long: 2 years of anorexia, 10 years bulimia and long-term use of antidepressants and tranquilizers.

Outcome of my adventures with RPP – 20 years ago I was diagnosed with impaired gastrointestinal motility (gastroparesis) – after many years of anorexia and bulimia (10 years of cleansing and laxative abuse). It is a common and life-threatening complication of an eating disorder. It causes symptoms such as nausea, vomiting, severe gastroesophageal reflux disease, regurgitation, bloating, water retention, constipation, diarrhea, premature fullness, and more.This is hell, and the normal relationship with food for healthy people becomes a big problem: eating too often, eating certain food groups, eating too much food, or even eating at all can cause vomiting, severe pain or severe nausea. “

People with impaired motility or gastroparesis for a long time cannot empty the stomach, which means that they take much longer (from several hours to several days) to digest food than for an ordinary person, due to the partially paralyzed digestive tract.

How do people with eating disorders and motor impairments reconcile recovering from an eating disorder and living gastroparesis?

“At the most painful moment from a medical point of view, I could not digest anything – I could not be SATURATED – I could not panic. It was not only the fear of calories, fear of gaining weight, but also terrifying, maddening SATURATION (another the mystical version of my psychotherapist, that the reason for this physical state: “I cannot accept my father” – broke down on all the physical processes in the gastrointestinal tract).Now I, being a completely healthy person, able to digest: lamb, cake, butter and any other products, I can call SATURATION, and then I called it HEAVY.

I wanted to eat more than anything else, I wanted to leave another hospital, mentally I wanted to overcome my bulimia, but could not because of motor impairment. I was tormented by bloating after every meal, sometimes vomiting; I didn’t go to the bathroom for several weeks, my stomach was swollen from every meal, and the pain was so bad after most of the meals I couldn’t get out of bed and breathe.Then I thanked another psychotherapist for their help, said that everything was ok, that I was healthy, and went home – again for bulimia and laxatives. And then I felt physically good. It was almost impossible to be well fed. Either baby food or bulimia – that’s the only way I could get rid of gastroparesis. Gastroparesis was the result of my years of RIP, not the cause. I didn’t know what happened to me for many years. Because it was impossible at that time to unite the doctors into one that my Gastroparesis is a consequence of my RPP and that everything should be treated together.Indeed, 20 years ago there was no such specialization as a specialist in the field of RPE.
The psychotherapist had no experience in gastroenterology, dietetics, and the gastroenterologist had no education in Psychology. The circle is complete. “

Most eating disorder programs in Europe, the United States and even more so in Russia are not designed to treat people with gastrointestinal or chronic illnesses, even if they are complications of eating disorders.And if you look at the statistics of our work and the number of clients over 17 years, then almost 98% had all the above described symptoms, someone had more, someone less, but they were, and these problems with the gastrointestinal tract interfered with the therapy of bulimia and anorexia with classical psychotherapy or independent attempts to recover at home.

And this is one of the most difficult problems on the road to recovery from RPF. Combine the treatment of Gastroporesis with the recovery from bulimia and anorexia. We often write that antidepressants do not help in therapy because they do not work with the gastrointestinal tract, do not create eating habits consciously, do not teach to understand food and listen to the work of your stomach: which food is right for you and which is not, and with what food still has to train.Yes, for 1 or 2 months, antidepressants can help: calm down, sleep, that is, relieve tension caused by prolonged hunger, fear of food and obsessive thoughts about food, but when issues with SATURATION are not resolved, she is not accustomed, a new eating habit is not created , the relationship with food is not established, then after a while the RPP returns again. But statistics can arise in this way. The patient received antidepressants, the breakdowns were gone, the psychotherapist was happy, Fluoxetine, aka Prozac, too, the client happily thanked him and left.But you need to start eating and eating in an adult way, alone, in your apartment, seriously, eating with gusto: main courses, “scary” soups too, and also birthdays, weddings and funerals, restaurants and pizza. And SATURATION is unbearable. Then everything is new.

For many, it takes a couple of months to restore the work of the gastrointestinal tract, for some for six months, and for others for years. It all depends on the type and duration of the disease, as well as the personal characteristics of the patient.

I thought that treating gastroparesis and eating disorders together in one treatment program would be the best solution.Treat both diseases at the same time. This practice in my therapy helps most people get the treatment they need for ADR and not fall out of order when Satiety appears.

For many, recovering from an eating disorder really means learning to eat freely again. But for me, as someone who fought on my own 20 years ago with motor impairment, this is not entirely true. For me, recovery is an opportunity to sit quietly with food in my stomach, cope with uncomfortable physical sensations, pain in the gastrointestinal tract, go through waves of anxiety and guilt, and forget about these feelings at the table.For me, convalescence is a physical calm experience of Satiety. My view of recovery is different from many eating disorder treatment programs.

It takes a little longer to treat Bulimia with gastroparesis, but it can be cured with a little patience, but these expended forces will definitely pay off, because at the end of your work you will get a calm stomach, comfort from satiety, emotional and conscious freedom from food, get off from a sugar needle and get for all this health and a slim or thin body (as you like :))

If you need support, call +7 (903) 098-77-55 (WhatsApp) or write by e-mail info @ bulimii.net. Specialists RARPP will help you cope with bulimia and you can start a new life without an eating disorder as soon as possible.

SIGN UP FOR A CONSULTATION WITH A SPECIALIST ON RPP

Gastroparesis | ehlersdanlos

Gastroparesis (gastric paresis)

What is gastroparesis?

Gastroparesis, also called “delayed gastric emptying”, is a condition in which the stomach takes much longer to digest its contents.Typically, the stomach muscles move food into the small intestine for further digestion. The vagus nerve controls the movement of food from the stomach through the digestive tract. Gastroparesis

occurs when the vagus nerve is damaged and the muscles in the stomach and intestines are not working properly. Therefore, food moves slowly or stops moving through the gastrointestinal tract.

What causes gastric paresis?

Diabetes is the most common cause of gastroparesis.People with diabetes have high blood glucose, also called blood sugar, which in turn causes chemical changes in the nerves and damage to the blood vessels that carry oxygen and nutrients to the nerves. Over time, high blood glucose levels can damage the vagus nerve.

Some other causes of gastroparesis:

– surgery on the stomach or vagus nerve
– viral infections
– anorexia nervosa or bulimia
– anticholinergic medications – they slow down bowel movements
– gastroesophageal reflux disease
– smooth muscle disorders such as amyloidosis and scleroderma
diseases of the nervous system, including abdominal migraine and Parkinson’s disease
– metabolic disorders, including hypothyroidism

Many people have what is called idiopathic gastric paresis, that is, the cause is unknown and cannot be found even after medical tests …

What are the symptoms of gastroparesis?

– heartburn
– pain in the upper abdomen
– nausea
– vomiting of undigested food, sometimes several hours after eating
– early satiety
– weight loss due to poor absorption of nutrients or low calorie intake
– bloating
– high and low blood glucose levels
– lack of appetite
– gastroesophageal reflux cramps in the abdominal region

Solid foods high in fiber such as raw fruits and vegetables, fatty foods, or drinks high in carbon dioxide may promote development these symptoms.
Symptoms of gastroparesis can be mild or severe, depending on the individual. Many people with gastroparesis experience a wide range of symptoms, making it difficult for even a doctor to diagnose.

What are the complications of gastroparesis?

If food stays in the stomach for too long, it can cause bacterial growth as a result of food fermentation. In addition, food can harden and turn into a hard mass called bezoar, which can cause nausea, vomiting, and stomach obstruction.Bezoars can be dangerous if they block the passage of food in the small intestine.

Gastroparesis can worsen the course of diabetes, making it more difficult to control blood glucose levels. When the food that was in the stomach finally enters the small intestine and is absorbed, blood glucose levels begin to rise. Gastroparesis makes gastric emptying unpredictable, and a person’s blood glucose levels can also be unpredictable and difficult to control.

How is gastroparesis diagnosed?

After a complete medical examination and based on your medical history, your doctor may order several blood tests to check the chemistry and electrolyte levels.To rule out other disturbances, the doctor may perform the following tests:
– Upper endoscopy.
– Ultrasound.
– X-ray with barium.

Once other causes have been ruled out, the doctor will perform one of the following tests to check gastric emptying to confirm the diagnosis of gastroparesis.

– Scintigraphy gastric emptying. This test involves ingesting soft food, such as an egg, that contains a small amount of a radioactive substance called a radioisotope, which is shown on a scan.

The radiation dose from radioisotopes is not dangerous. The rate of gastric emptying is measured diagnostically at 1, 2, 3, and 4 hours. When more than 10% of the food is still in the stomach after 4 hours, the diagnosis of gastroparesis is confirmed.
– Check for exhalation. After ingestion of food containing small amounts of the isotope, breath samples are taken to measure the presence of the isotope in carbon dioxide, which should not be present when a person exhales. The results show how quickly the stomach empties.
– SmartPill.Approved by the US Food and Drug Administration (FDA) in 2006, the SmartPill is a small, capsule-shaped device.

travels through the digestive tract and collects information about its movement, which is sent to a receiver that the patient must wear around the waist or neck. When the capsule is removed from the body after a couple of days, you take the receiver back to the doctor, who outputs the information to the computer.

How to treat gastroparesis?

Treatment of gastroparesis depends on the severity of the symptoms.Most gastroparesis is not treated – it is usually a chronic disease. Treatment helps you control it.

Treatment

Your doctor may try different drugs or combinations of drugs to find the most effective treatment. It is very important to discuss the risk of side effects of any medication with your doctor.

Metoclopramide (Cerucal). This drug stimulates the muscle contractions in the stomach to aid in emptying. Metoclopramide also helps reduce nausea and vomiting.Metoclopramide is taken 20 to 30 minutes before meals and at bedtime. Side effects of this drug include fatigue, drowsiness, depression, anxiety.
Erythromycin. This antibiotic also improves gastric emptying. It works by increasing the contractions that move food through the stomach. Side effects include nausea, vomiting, and abdominal cramps.
Domperidone. This drug works like metoclopramide to improve gastric emptying and reduce nausea and vomiting. The drug is restricted in the United States.
Other medicines. Other medicines can be used to treat the symptoms and problems associated with gastroparesis. For example, an antiemetic can help with nausea and vomiting. Antibiotics kill bacterial infections. If you have a bezoar in your stomach, your doctor may use an endoscope to inject medicine into it to dissolve it.

Diet.

Changing eating habits can help control gastroparesis. Your doctor or dietitian may prescribe six small meals a day instead of three large meals.If little food enters the stomach every time you eat, it will not be able to fill. In more severe cases, a diet of liquid or pureed food may be prescribed.
Your doctor may recommend that you avoid foods high in fat and fiber.

Feeding tube

If a liquid or mashed diet does not work, surgery may be required to insert the feeding tube. A tube called a jejunostomy is inserted through the skin on the abdomen into the small intestine.The delivery tube bypasses the stomach and puts nutrients and medications directly into the small intestine.

Parenteral nutrition

Parenteral nutrition – nutrients enter the bloodstream directly, bypassing the digestive system.

This approach is an alternative to jejunostomy and is usually temporary to get you through the difficult period with gastroparesis. Parenteral nutrition is used only for severe gastroparesis and if other methods have not helped.

Gastric electrical stimulation

A gastric neurostimulator is an implantable device that emits weak electrical impulses to help with nausea and vomiting associated with gastroparesis. This operation is applied to those people whose nausea and vomiting cannot be controlled with medication.

Botulinum toxin

Botulinum toxin use has been associated with improved gastroparesis symptoms in some patients; However, further research in this form of therapy is not required.

Points to Remember

Gastroparesis is the result of damage to the vagus nerve, which controls the movement of food through the digestive system. Instead of moving normally through the gastrointestinal tract, food is trapped in the stomach.
Gastroparesis can occur in people with type 1 diabetes or type 2 diabetes. The vagus nerve is damaged after years of high blood glucose levels, resulting in gastroparesis. In turn, gastroparesis contributes to impaired blood glucose control.
Symptoms of gastroparesis include early satiety, abdominal pain, abdominal cramps, heartburn, nausea, vomiting, bloating, gastroesophageal reflux, lack of appetite, and weight loss.
Gastroparesis is diagnosed by tests such as x-rays, manometry and gastric emptying scans.
Treatment includes dietary changes, oral medications, jejunostomy, parenteral nutrition, gastric neurostimulant, or botulinum toxin.

90,000 Bulimia Treatment

Striving for beauty, slimness and normal weight is quite natural for a person.But sometimes it becomes so severe that it develops into an eating disorder – bulimia .

According to statistics provided by the US National Institute of Mental Health, Bulimia nervosa affects one in 100 adults. Most often, young women, but the disorder can occur in a person of any gender and age.

Bulimia has two types of symptoms:

• Constant overeating .At one time, a person can eat 2000 kcal. This is almost a daily rate.
• “Cleaning” – usually follows immediately after a meal. Most often, a person tries to induce vomiting. Some use laxatives, diuretics, and exhaust themselves by exercising in the gym.

Bulimia is a constant movement in the cycle of “overeating-cleansing”. More precisely, not even in a circle, but in a spiral. The body experiences a great load, stress from this. Health deteriorates over time.Bulimia is a dangerous disease that requires treatment. Clinic Cordia employs experienced professionals who know how to help. Call: Make an appointment around the clock. Call +7 (495) 268-09-02

“How to understand that my loved one suffers from bulimia?”

Most often, the person himself is not fully aware of the painfulness of his condition. In his understanding, the main problem is excess weight, with which you need to fight. Constant overeating and “cleansing” are accompanied by feelings of awkwardness, shame, psychological complexes.Therefore, a person tries to hide the problem from others. If people lose weight with anorexia, then with bulimia the weight is often kept within normal limits. This makes it even more difficult to recognize the disease.

There are some alarm bells. They signal that your loved one may have an eating disorder and it’s time to see a doctor :

• A person is fixated on weight loss, dieting, maintaining a slim figure. He just talks about it.
• You constantly notice food leftovers in the trash can, in the kitchen: candy wrappers, snack bags, fruit peels. There are too many of these “evidences”, suspiciously many.
• After eating, a person runs to the bath or to the toilet, and generally spends a lot of time there. Sometimes you smell vomit there.
• Often times, people with bulimia try fancy diets, literally become obsessed with healthy eating, and avoid certain foods.
• Bulimic patients avoid eating in the presence of other people, in public places.They eat in secret.
• A person is very shy about his real or contrived fullness, hiding it under baggy clothes.
• Often, frequent emotional swings and sleep disturbances are added to the strangeness in behavior.

Did you find a loved one or yourself with symptoms from this list? See a specialist. Bulimia not only lowers the quality of life – it leads to complications that can be dangerous.

Why is bulimia dangerous?

It seems to the patient that he is constantly overeating, in fact, due to constant “cleansing” and fanciful diets, the body does not receive nutrients.Many people with bulimia experience headaches and dizziness. The skin becomes thin, the nails are brittle. Immunity decreases, wounds on the skin heal worse.

Due to constant fluctuations in weight and deterioration of the digestive system, metabolism is disturbed. Artificial vomiting and uncontrolled intake of laxatives cause the body to lose water and electrolytes. The heart suffers, it is fraught with arrhythmia and heart attack. Acid during vomiting damages teeth, they quickly deteriorate.

Bulimia can lead to gastroparesis – a condition in which the muscles in the stomach wall stop contracting normally. Concerned about heartburn, belching, nausea. Decreases appetite, the patient loses weight. In the worst case, overstretching of the stomach leads to rupture of its wall – the outcome of this complication can be fatal.

In women, metabolic disorders lead to menstrual disorders and infertility.

The sooner you see a doctor, the better.In advanced cases, bulimia leads to disorders that will persist even after the normalization of eating behavior, and they will have to be dealt with for a long time.

Why does bulimia occur?

The causes of the disorder are not fully understood. It is believed that both genetics and lifestyle, outside influences are involved. Usually the first symptoms appear after one of the provoking factors has arisen in a person’s life:

• Severe stress, traumatic events.
• Alcohol and substance abuse.
• Strong feelings of real or contrived fullness, low self-esteem.
• Work in an area where appearance is very important, for example, in the modeling business.

Although the causes of bulimia are not well understood, modern doctors know how to successfully combat this disorder and can help you .

Bulimia Treatment

Fighting the disorder is built on three pillars:

1. During sessions of individual psychotherapy , the specialist helps to break the cycle of “overeating-cleansing”, get rid of negative thoughts about weight and appearance, and eliminate emotional problems.
2. Group therapy often works well when patients come together, share their experiences, support and motivate each other.
3. Antidepressants help some patients.

Sometimes inpatient treatment is required. Doctors in the hospital help to cope with some conditions:

• If a person often artificially induces vomiting, over time the body “gets used” to it, and it occurs reflexively after each meal.
• If the patient is taking psychoactive substances, doctors will detoxify.
• If the person is severely malnourished, they may need intravenous or tube feeding.

The doctors at the Cordia Clinic are highly experienced in the treatment of bulimia and other eating disorders. We know how to return you or your loved one to a normal life, free from constant overeating, painful thoughts about your weight, figure. We’ll tidy up your relationship with food.Contact us:

Nausea, vomiting

1. Home
2. Symptoms
3. Nausea, vomiting

Nausea – An unpleasant sensation in the stomach and / or throat, which often leads to vomiting.

Vomiting – the release of the contents of the stomach (and / or duodenum) through the mouth.

Causes of nausea and vomiting

Nausea and vomiting may occur separately or together.

Most common causes of nausea and vomiting:

• Gastroparesis (a condition in which the muscles of the stomach wall do not push food further into the intestine, interfering with digestion)
• Rotavirus infection
• Gastritis (inflammation of the stomach lining)
• Viral gastroenteritis (stomach flu)
• Appendicitis (inflammation of the appendix)
• Duodenitis (inflammation of the initial part of the small intestine)
• Intestinal obstruction (the presence of an obstruction in the intestines to pass the stool)
• Intestinal paresis (impaired bowel movement)
• Intestinal ischemia (impaired blood supply to the intestine)
• Conducting chemotherapy
• General anesthesia

Other possible causes of nausea and vomiting:

• Drinking too much alcohol
• Anaphylaxis (in children)
• Anorexia nervosa
• Vestibular neuritis
• Benign paroxysmal positional vertigo
• Brain tumor (benign or malignant)
• Bulimia
• Concussion
• Cholecystitis
• Cyclic vomiting syndrome
• Depression
• Dizziness
• Diabetic ketoacidosis
• Ear infections
• Food poisoning
• General anxiety disorders
• Gastroesophageal reflux disease
• Hernia of the esophageal opening of the diaphragm
• Heart failure
• Cholelithiasis
• Fever (in children)
• Hydrocephalus (congenital pathology of the brain)
• Hyperparathyroidism (overactive parathyroid hormone)
• Hyperthyroidism
• Hypoparathyroidism (decreased function of the parathyroid glands)
• Motion sickness
• Enlarged spleen (splenomegaly)
• Intracranial hematoma
• Migraine
• Pregnancy
• Liver cancer
• Hepatic failure
• Taking medications (including aspirin, nonsteroidal anti-inflammatory drugs, oral contraceptives, digitalis drugs, drugs and antibiotics)
• Meniere’s disease
• Meningitis
• Milk allergy (in infants and children)
• Pancreatic cancer
• Pancreatitis
• Stomach ulcer
• Encephalopathy
• Pyloric stenosis (in infants)
• Radiation therapy
• Severe pain
• Traumatic brain injury

Our specialists

All specialists

90,000 Gastroparesis – iValueHealth.NET

Gastroparesis

Abdomen | Gastroenterology | Disease

Description

A person with gastroparesis has a chronic condition in which the stomach takes longer than usual to push food into the small intestine. The main symptoms of gastroparesis are nausea and vomiting. Other symptoms of gastroparesis include abdominal pain, bloating, early satiety, and in severe cases, weight loss by reducing food intake due to symptoms.Reducing food intake, and limiting the types of food that are eaten, can lead to nutritional deficiencies.

Vomiting with gastroparesis usually occurs after eating; however, with severe gastroparesis, vomiting can occur without food. The characteristic vomiting occurs several hours after a meal, when the stomach is maximally distended by the presence of food and secretions stimulated by the intake of food.

Causes and risk factors

Gastroparesis is caused by damage to the vagus nerve, which stimulates the abdominal muscles to contract.