The Different Tests to Diagnose Gastroparesis

There are may different tests to confirm the diagnosis of Gastroparesis. I wanted to write an article to list the different methods doctors can use to determine whether or not you have Gastroparesis. Sometimes, multiple tests are needed. Speak with your doctor before you are tested, just in case you are on any medications which can skew the test results (i.e. opiates like hydrocodone can slow down motility and prevent you from receiving an accurate diagnosis.

The first test I want to discuss is the breath test, which can be used to determine if someone has Gastroparesis or not. I have never been tested using the breath test method, so I researched the topic to understand it as well as to write about it.


Testing for Gastroparesis: The Breath Test


According to the US PHARMACIST,

"Gastric Emptying Breath Test

Kendra L. Sutton, PharmD Candidate
Florida A&M University
College of Pharmacy
Tallahassee, Florida

Cy D. Sims, PharmD Candidate
Florida A&M University
College of Pharmacy
Tallahassee, Florida

Marlon S. Honeywell, PharmD
Professor of Pharmacy Practice
Florida A&M University
College of Pharmacy
Tallahassee, Florida

Ellen Campbell, PhD
Associate Professor of Economic, Social and Administrative Pharmacy
Florida A&M University College of Pharmacy and Pharmaceutical Sciences
Tallahassee, Florida

Tracy A. Thomas, PT, PhD
Associate Professor of Physical Therapy
Florida A&M University
Tallahassee, Florida

Eboni Allen, MSN, ARNP-C
Bond Community Health Center
Tallahassee, Florida

Anneka J. Gaffney, MSN, ARNP-BC
Bond Community Health Center
Tallahassee, Florida

Temple Robinson, MD
Chief Medical Officer
Bond Community Health Center
Tallahassee, Florida

U.S. Pharm. 2015;40(12):HS36-HS40.



​Delayed gastric emptying, also known as gastroparesis, is a disorder that either slows or stops movement of food through the gastrointestinal (GI) tract. It commonly causes nausea, vomiting, heartburn, erratic blood glucose levels, and postprandial fullness.1 Normally, the smooth muscles of the GI tract move food down to the stomach and through the intestines, where it is excreted through the rectum. This process is controlled by the vagus nerve, a component of the parasympathetic nervous system. The most common causes of gastroparesis are diabetes mellitus and surgery; it may also be of unknown cause. Diabetes accounts for almost one-third of cases of gastroparesis, with about 5% to 12% of all diabetes patients experiencing this disorder.2,3 Diagnosis is most often determined by performing endoscopy or using scintigraphy—a specialized radiologic imaging technique—to measure the rate at which radioactive food passes through the GI tract. The Gastric Emptying Breath Test (GEBT) makes it possible to diagnose gastroparesis without the use of radioactive materials.




Gastric Emptying Breath Test

Developed by Advanced Breath Diagnostics, the GEBT is a non-radioactive test that utilizes carbon-13 (13C). Labeling with 13C stable isotope is essentially safe, as 1.1% of our bodies, and of the food we eat, consists of 13C; the remaining 98.9% consists of 12C.4 The GEBT test was developed for adult patients who are symptomatic for gastroparesis. The test measures the rate of gastric emptying of solids and aids in the diagnosis of gastroparesis. The test system utilizes a gas isotope ratio mass spectrometer for the measurement of the ratio of 13CO2 to 12CO2 in breath samples. Administration of the GEBT does not require a special facility, but it should be administered under the guidance of a healthcare professional.4 The GEBT is shown in FIGURE 1.

Source: in article



​
Test Administration

The GEBT is measured over a 4-hour time cycle. Detailed administration instructions can be found in Table 1. Multiple breath samples are obtained from the patient; sampling should be performed subsequent to an 8-hour fast. After providing multiple premeal breath samples (Table 2), the patient consumes the standard GEBT meal consisting of pasteurized scrambled egg mix containing a dose of 43 mg of 13C-Spirulina, 6 saltine crackers, and 6 ounces of potable water.5 The 13C-Spirulina is eventually passed through the GI tract to the intestines; it is in the intestines that the Spirulina is absorbed and metabolized to the 13CO2 expired in the breath. Single postmeal breath samples are subsequently collected (Table 2) at 45, 90, 120, 150, 180, and 240 minutes from the end of test-meal consumption. The post-meal breath samples are transmitted to a laboratory for assessment of 13CO2/12CO2 in each sample. By measuring the change in this ratio over time as compared to the pre-meal value, the rate of 13CO2 excretion can be calculated and the patient’s gastric-emptying rate determined.4,5 See FIGURE 2 for a diagram outlining the procedure.

Source: in article





Efficacy

Scintigraphy (The definition of Scintigraphy, according to the Dictionary,
"noun, MEDICINE. A technique in which a scintillation counter or similar detector is used with a radioactive tracer to obtain an image of a bodily organ or a record of its functioning."), a competitor to the GEBT, utilizes a radioisotope that is unsafe for patients who are having multiple tests performed, pregnant women, women who breast-feed, and children. Scintigraphy also requires special equipment and a specific testing site, whereas the GEBT can be implemented outside the clinical setting and breath samples are subsequently sent to a laboratory for analysis.4-6

In a clinical trial comparing the GEBT and scintigraphy, the GEBT was shown to be comparable to scintigraphy. Researchers compared the results from both the GEBT and scintigraphy and found that GEBT results agreed with scintigraphy results 73% to 97% of the time when measured from various time points during the test.4,5 The GEBT was also found to be safer than scintigraphy.



Adverse Effects/Contraindications

In the comparative study mentioned above, 13 participants complained of adverse effects.5,7 Adverse events experienced were often considered mild; these events included nausea, heartburn, diarrhea, dry heaves, abdominal pain, acid reflux, dizziness, and head cold. It was also determined later that many of these events were not related to the device. Contraindications to use of the GEBT include egg, milk, or wheat allergy, as the food product ingested contains these ingredients.5,8 Additionally, as the digestion of the product involves other organs such as the pancreas and liver, the GEBT is not recommended in patients with malabsorption, or who have diseases such as pancreatitis or hepatitis.



Conclusion

The GEBT is unique in that it provides a nonradioactive, noninvasive, orally administered product that performs as well as scintigraphy. The ease of use outside of the clinical setting also makes this device an attractive alternative to other available tests. For more information, contact Advanced Breath Diagnostics at (615) 376-5464.

REFERENCES
1. National Institutes of Health. National Institute of Diabetes and Digestive and Kidney Diseases. Gastroparesis. June 2012. www.niddk.nih.gov/health-information/health-topics/digestive-diseases/gastroparesis/Pages/facts.aspx. Accessed July 10, 2015.
2. Soykan I, Sivri B, Sarosiek I, et al. Demography, clinical characteristics, psychological and abuse profiles, treatment, and long-term follow-up of patients with gastroparesis. Dig Dis Sci. 1998;43:2398-2404.
3. Bytzer P, Talley NJ, Leemon M, et al. Prevalence of gastrointestinal symptoms associated with diabetes mellitus: a population-based survey of 15,000 adults. Arch Intern Med. 2001;161:1989-1996.
4. Szarka L, Camilleri M, Vella A, et al. A stable isotope breath test with a standard meal for abnormal gastric emptying of solids in the clinic and in research. Clin Gastroenterol Hepatol. 2008;6:635-643.
5. FDA. Gastric emptying breath test. www.accessdata.fda.gov/cdrh_docs/pdf11/P110015b.pdf. Accessed July 21, 2015.
6. Parkman HP, Hasler WL, Fisher RS. American Gastroenterological Association medical position statement: diagnosis and treatment of gastroparesis. Gastroenterology. 2004;127:1589-1591.
7. Abell TL, Bernstein RK, Cutts T, et al. The American Motility Society Task Force on Gastroparesis. Treatment of gastroparesis: a multidisciplinary clinical review. Neurogastroenterol Motil. 2006;4:263-283.
8. Park M, Camilleri M. Gastroparesis: clinical update. Am J Gastroenterol. 2006;101:1129-1139.
9. Gastric Emptying Breath Test [package insert]. Brentwod, TN: Advanced Breath Diagnostics, LLC; 2015.

To comment on this article, contact rdavidson@uspharmacist.com."

This was written in May of 2015 by DIATRIBE LEARN,

"The FDA recently announced the approval of the Gastric Emptying Breath Test (GEBT) as a diagnostic tool for gastroparesis – this condition is, though not as well known, a common complication of diabetes. Gastroparesis slows or stops the movement of food down the digestive tract from the stomach to the small intestine – this is caused by problems with stomach muscle contractions, which usually help move the food forward. In other words, digestion doesn't go nearly as well as it should. The GEBT works by measuring carbon dioxide in a patient’s breath over a four-hour period after eating a 'test meal.' The carbon dioxide measurement is used to calculate the rate at which food is emptied from the stomach.

GEBT should offer a major improvement over the current gold standard for gastroparesis diagnosis, gastric emptying scintigraphy. Gastric emptying scintigraphy requires eating radioactively labeled foods and measuring their digestion with an external scanner. As the GEBT does not require imaging equipment or training for the handling of radioactive materials, the hope is that it will be easier for more health care providers to use in their practices. A clinical study of 115 people conducted to support GEBT’s approval demonstrated that results from the GEBT agreed with the results of scintigraphy 73%-97% of the time.

Gastroparesis is a fairly common complication of diabetes, impacting an estimated 40% of type 1 and 30% of type 2 patients. In addition to causing symptoms like nausea and heartburn (see a full list of symptoms here), gastroparesis can make managing diabetes much more difficult, as it can lead to increased blood glucose variability and hypoglycemia. Gastroparesis remains an area of significant need, as no new therapies have been approved in the US in over 30 years and dietary interventions have not been clearly demonstrated to work. The approval of the GEBT is a positive step towards increased detection of this complication; for more information on diabetes and gastroparesis, please see the ADA’s page on it here. –AJW/ER"

Source: https://www.researchgate.net/figure/Methods-for-GE-assessment-by-breath-test-T-1-2-B-and-scintigraphy-T-1-2-S-and_fig1_251569573




Testing for Gastroparesis: The Smart Pill Test

I have already written about this before (in 2012), but was speaking about my own experiences with The Smart Pill Test. At the time I wrote this article, there was not a lot of information online about Gastroparesis, much less the different tests used to diagnose someone who has Gastroparesis.

Therefore, I wanted to put all of the testing I am aware of, to determine Gastroparesis, in the same article. The link to my article about The Smart Pill Test can be found here: http://www.emilysstomach.com/2012/08/smart-pill.html





Furthermore, GASTRO CURE says this about The Smart Pill,

"GI MONITORING SYSTEM
SmartPill is an ingestible, wireless capsule that measures pressure, pH and temperature as it transits the GI tract. This information is used to provide regional transit times including gastric emptying time, small bowel transit time, colonic transit time, combined small/large bowel transit time, whole gut transit time, pressure contraction patterns from the antrum and duodenum and motility indices.

Administered in the physician’s office, the SmartPill test is completely ambulatory and allows the patient to go about their normal routine during the course of the test. As the SmartPill Capsule passes through the GI tract, it transmits data to a SmartPill Data Receiver worn by the patient. Once the single-use capsule has passed from the body, the patient returns the data receiver to the Physician who then can download the collected data to a PC. The Physician then uses SmartPill’s MotiliGI software to display and analyze the data, providing the physician with test results in both graphical and report formats.



The SmartPill Wireless Motility Capsule

The SmartPill Capsule transits the intestines by peristalsis, or the normal rhythmic contraction of the intestinal muscles, and is capable of transmitting data continuously for at least five days. The single-use capsule is excreted naturally from the body, usually within a day or two.



SmartPill Data Receiver & Docking Station

The battery-operated SmartPill Data Receiver collects and stores the test data. The Receiver is capable of transmitting data for real-time monitoring of a test. It also stores a complete record of the data captured by the SmartPill Capsule for download to a PC after the test is complete.

The SmartPill Data Receiver must be worn by the patient for the duration of the test on a belt clip or a lanyard around their neck. The data receiver may be removed for sleeping or bathing but should be kept in close proximity at all times.

After completion of the test, the SmartPill Data Receiver is connected to the system computer using the SmartPill Docking Station. The docking station features an industry standard USB type 2.0 interface that is used to transfer captured data to the PC for analysis and data reconstruction using SmartPill’s MotiliGI software. The data analysis can be performed at the convenience of the physician in a single session or during multiple sessions without the need for the patient to be present.



SmartPill MotiliGI Software

SmartPill MotiliGI software comes pre-installed on the system PC and provides an graphical user interface. MotiliGI receives and processes data from the SmartPill Data Receiver, stores the data in a file on the system PC, provides a test summary and report, graphs for display purposes, and shows the data values captured during the SmartPill test. MotiliGI provides powerful data analysis tools, and affords the user a variety of test reporting and exporting options.



System Computer

The SmartPill GI Monitoring System is supplied with a personal computer which hosts MotiliGI software and supports communication between MotiliGI and the data receiver and docking station.



SmartPill Activation Fixture

The activation fixture contains very powerful magnets and is used to activate and deactivate the SmartPill Capsule."

Source: http://gastrocure.com/smart-pill/



I wanted to update this a bit since there is A LOT more information about The Smart Pill Test than when I was first diagnosed. For instance, I did not know that The Smart Pill Test could not work with certain conditions, like Crohn's Disease. So, I have actually learned a lot of new things about The Smart Pill test that I was unaware of before.


According to HEALTH ESSENTIALS,

"Gastroparesis: ‘Smart’ Pill Uncovers This Mysterious Stomach Condition: Data-Gathering Pill Moves Through Your GI Tract

If you have unexplained stomach problems, such as nausea, bloating, constipation, chronic abdominal pain or vomiting, you might swallow a pill — but not the medicated kind.

Instead, consider a 'smart' pill, which gathers data as it moves through your GI tract. This painless tool helps your doctor pinpoint the cause of your problem so you can get the best treatment, says gastroenterologist Michael Cline, DO.




How can the pill help?

Data gathered by such a pill could help your doctor diagnose a condition called gastroparesis, which causes food to move abnormally slowly from your stomach to the small intestine, while ruling out another GI condition, such as chronic constipation.

Gastroparesis, which means partial paralysis of the stomach, is a common condition for those with diabetes. The condition reduces your stomach’s ability to empty its contents, but it does not involve a blockage.

'Basically, gastroparesis is a stomach that doesn’t empty well,' says Dr. Cline.

And it’s a difficult disease to treat, he says. Treatment typically begins with adjustments to diet and medication. If those approaches don’t work, surgical treatments are the next steps.




How does the pill work?

The SmartPill® provides a simple, painless way to collect data about your GI tract without using radiation, Dr. Cline says. It’s an FDA-approved, disposable capsule that you swallow.

'It’s called ‘smart’ because it measures the acid level, the pressure level, the temperature and time of your GI tract,' he explains. 'It’s similar to the pill cam, which takes pictures inside your body. This is its sister, essentially.'

Instead of taking photos of the inside of your body, the SmartPill measures motility and movement of your gut. It wirelessly transmits data about your GI tract to a recorder that you wear on a belt clip or lanyard around your neck as you go about your daily activities.

'The recorder captures the data and we download it into a computer and print out what’s happening, from start to finish,' Dr. Cline says. 'We can get all of this data and measurements of motility and movement without any wires attached and without X-rays.'

Depending on how slowly your intestines move, the SmartPill typically works its way through your system in three to five days. If you have normal motility, it is in your stomach for less than four hours, in your small intestine for less than six hours and in your large intestine or colon for less than 59 hours.

Source: HERE





Ruling out other GI issues

The SmartPill can also help a physician rule out other gastric issues that can cause problems in your small intestine or colon.

'You want to make sure that you’re dealing with just gastroparesis and not another issue,' says Dr. Cline.

The one real benefit of the SmartPill over everything else available is that it measures all three sections of your intestine with one test. Dr. Cline says that not only are you looking for gastroparesis, but you’re also looking at your small intestine movement and colon movement.

'There’s no other test out there that can measure all three with one test,' he says. 'I tell patients you get a lot more bang for your buck with the SmartPill.'




Is a ‘smart’ pill right for you?

The SmartPill does not work for people with certain conditions, Dr. Cline says. These conditions include:

A history of strictures in your intestines, such as scarring (which can narrow the bowel passage)
Inflammatory bowel disease, like Crohn’s disease
A heart pacemaker (or pacemakers in other organs)

'The main risk of the SmartPill is it could get stuck,' he explains. 'If you have normal intestines, the SmartPill will not stick. If the pill gets stuck, you have a problem, obviously. You don’t want to give a patient who is at a high risk of having narrowing bowels the SmartPill.'

The FDA advises against giving the SmartPill to patients who have pacemakers.

Dr. Cline says he also advises patients who need an MRI to delay taking the SmartPill.

'The final contraindication, which is pretty rare, is if the patient has an MRI scheduled,” he says. 'You obviously don’t want to do it until after the MRI is over. You can’t go through an MRI with that pill inside of you.'"

For more information about The Smart Pill, please visit:

https://www.medtronic.com/covidien/en-us/products/motility-testing/smartpill-motility-testing-system.html

http://www.pain.ucdavis.edu/internalmedicine/gastro/smartpill.html

https://www.g-pact.org/gastroparesis/testing/smartpill




Testing for Gastroparesis: The Gastric Emptying Study

In February of 2013, I wrote an article about the Gastric Emptying Study and my experience doing the test. You can read about my experience in my article, along with pictures I took, documenting the testing, here: http://www.emilysstomach.com/2013/02/day-two-of-mayo-clinic-gastric-emptying.html


UW MEDICINE explains the Gastric Emptying Study,

"What is a gastric emptying scan?

​​ A gastric emptying scan (GES) is a nuclear medicine exam that uses a radioactive material that you will eat in a meal. You will eat this meal in the Radiology department before your scan. The radioactive material allows doctors to see how your stomach empties.

This scan is used to help diagnose conditions called motility disorders.​ These are conditions that change the way the stomach contracts and moves food into your intestines. A GES is a form of radiology, because radiation is used to take pictures of your body.



How does the scan work?

A gamma camera takes pictures as the radioactive food moves through your stomach. The camera detects the gamma rays emitted from the food. A computer then produces pictures and measurements of your stomach.



How should I prepare for the scan?

You will need to fast for 6 hours before the scan.

If you smoke, do not smoke the morning of the test and during the hours of the scan.

If you are a woman and you are still menstruating, it is best to have your scan done in the first 10 days of your menstrual cycle.



Do not take these drugs for at least 2 days before your test, unless your doctor tells you otherwise:

​​Drugs called prokinetic agents that speed up the motility of your GI tract. Some of these are metoclopramide (Reglan), erythromycin, tegaserod (Zelnorm), and domperidone (Motilium).

Drugs called anticholinergic antispasmodic agents that slow down the motility of your GI tract. Some of these are Bentyl, Donnatal, Levsin, Robinul, and Hyosyne.

Pain medicines called opiate analgesics. Some of these are codeine, demerol, Percocet (Oxycodone), Tylenol #3, Tylox, Oxycontin, Percodan, Fentanyl patch, morphine, Methadone, Vicodin (Hydrocodone), and Ultram (Tramadol).

Marijuana.

Do not take any laxatives the day before or any time during the test.

Note: It is OK to take relaxants(called benzodiazepines)such as Ativan, Valium, Librium, Xanax, and others. It is also OK to take anti-nausea medicines (called phenothiazines) such as Thorazine, Compazine, Phenergan, and others. These drugs do not affect gastric emptying.


You may take all other medicines the day of your test with small sips of water. Take these at least 2 hours before your test begins.


If you have severe nausea on the day of your test, we may give you medicine to reduce your nausea.



If You Have Diabetes

On the day of the test:

Your fasting blood glucose should be less than 275 mg/dL. A technologist will check your blood glucose before your test starts.

Please bring your insulin or other diabetes medicine with you. You may need to take it with your gastric emptying meal.



How is the scan done?

You will be given 2 small sandwiches, one filled with jam and one filled with 4 cooked egg whites that have been injected with a small dose of radioactive material. You will be asked to eat the sandwiches and drink water within 10 minutes. The egg will taste just like a regular egg. If you are allergic to eggs or wheat, please tell the person you schedule your appointment with. A different meal will be used.

After eating, you will be asked to lie flat on your back while the gamma camera take a picture of your stomach. You must lie still when the camera is taking pictures. If you move, the pictures will be blurry and may have to be taken again.



What will I feel during the scan?

Lying still on the exam table may be hard for some patients. The technologist will help make you comfortable.



How long will the scan take?

From start to finish, your gastric emptying scan will take about 4 hours.



There are 4 parts to the test:

First half hour: Eat meal, then take pictures with gamma camera (pictures take 5 minutes)
1 hour after meal: Take pictures (5 minutes)
2 hours after meal: Take pictures (5 minutes)
4 hours after meal: Take pictures (5 minutes)



After eating the meal:

​You may leave the Nuclear Medicine department between the times you have the pictures taken.

Do not eat or exercise until after the last set of pictures has been taken.



Who interprets the results and how do I get them?

When the test is over, the nuclear medicine doctor will review your images, write up a report, and talk with your doctor about the results. Your doctor will talk with you about the results and your treatment options."

Source: My own photo





According to HEALTH LINE (which has great information about the test and alternatives) also has information about Gastric Emptying Scans for children,

"Gastroparesis symptoms in children are similar to those seen in adults. Ask your doctor to administer this test to your child if they’re experiencing any of symptoms mentioned earlier.

The test for older children is identical to the test given to adults. If your child is a baby or infant, your doctor gives your child the radioactive food in milk or formula in an exam known as a milk study or liquid study. In this case, you may be instructed to bring your own formula or milk from home to make sure your child doesn't have an allergic reaction.

The radioactive substance is just as safe for your child as it is for an adult. The test usually takes about three hours for children. If your child is given the liquid study instead, the camera takes continuous images for about an hour. It’s important that your child remains still throughout the test. Make sure that you find a way to keep them occupied or calm before and during the test so that the results can be delivered smoothly.


The following items may help keep your child relaxed:

music
toys
movies
books
comfort objects, such blankets or pillows"

Source of a Gastric Emptying Scan: HERE





Testing for Gastroparesis: The Heidelberg pH Diagnostic Test

This test is very similar to The Smart Pill Test. I wrote about this test in August. You can read my blog article about it here: http://www.emilysstomach.com/2018/04/heidelberg-ph-test.html. I also included an excerpt below:

"What is a Heidelberg pH Test?

The Test will accurately verify the presence of a common Digestive Disorder

The Physician will require a complete Medical History before the Test

There will be a Transceiver that is placed over the Patient’s stomach during the test.

The pre test instructions will help achieve the most accurate results.

There is no discomfort during a Heidelberg pH test. Patients are relaxed and comfortable.

Remember to grab a good old fashioned distraction to pass the time.

Due to wireless interference, cell phones and personal electronic devices may need to be powered off.

The results are immediate so the Physician may have the post test consultation the same day.




Heidelberg pH Diagnostic Test will accurately verify the presence of low stomach acid production, high stomach acid production, no acid in the stomach, Dumping Syndrome, Acute or sub Acute Gastritis, Heavy Mucus in the stomach, and Pyloric insufficiency.

The Test is accomplished by measuring the time it takes for the acid producing cells (Parietal Cells) in the stomach to produce the required Hydrochloric acid. The strength of the acid (pH) is also measured during the test.

Patients are required to complete a consent form for the Physician’s Office Staff. If you have reservations about having a pH test, please discuss them with the Physician. Mental anguish and stress will only alter the test results.

The Technician will calibrate the pH Capsule to ensure it accurately records the pH values. The Technician will then place a transceiver over the Patient’s stomach. The transceiver receives and transmits the information from the pH Capsule and sends it wirelessly to the computer where the information is displayed. The nurse will rinse the pH Capsule and give it the Patient to swallow with a sip of water.

There is no discomfort during a Heidelberg pH Test. Patients are asked to relax and get comfortable while the test is being done. Remember to grab a good old fashioned distraction to pass the time.

Results are ready for the Physician to review as soon as the Technician ends the Test. Many Physicians opt to have a post test consultation as soon as the test is complete. In many cases the doctor will establish a treatment protocol on the same day. In many instances, after testing and treatment, patients stated that they feel better and healthier in just two or three days.


Unlike other procedures, the Heidelberg pH diagnostic test is an in-office procedure that does not require sedation or the use of a stomach tube.

There is no trauma or discomfort associated with our test, and the results of the Heidelberg test are available to the doctor as soon as the test is complete."

Source:HERE




Testing for Gastroparesis: The pH Bravo Test

I have had this test done as well. After I was first diagnosed with Gastroparesis, my doctor sent me to the Mayo Clinic to meet with a motility specialist there. I had to go off all of my other medications for a month before the doctor at Mayo would even see me, as I have mentioned before.

My personal experience was in February of 2013, and you can read the article here:

http://www.emilysstomach.com/2013/02/mayo-clinic-day-four-bravo-test.html

But, I want to discuss the test because the test now is a bit different than when I took it in 2013. Even though it is used as testing for GERD, my personal test found fifty-five events in twenty-four hours, with forty-six of them being vomiting. So, it might measure for GERD but my test was used to prove my vomiting with Gastroparesis, and how much I vomit.

Source: HERE





According to the CLEVELAND CLINIC,

"How does the Bravo esophageal pH test work?

A small capsule, about the size of a gel cap, is temporarily attached to the wall of the esophagus during an upper endoscopy. The capsule measures pH levels in the esophagus and transmits readings by radio telecommunications to a receiver (about the size of a pager) worn on your belt or waistband. The receiver has several buttons on it that you will press to record symptoms of GERD such as heartburn (the nurse will tell you what symptoms to record). You will be asked to maintain a diary to record certain events such as when you start and stop eating and drinking, when you lie down, and when you get back up. This will be explained by the nurse.



How do I prepare for the Bravo esophageal pH test?

Let your physician know if you have a pacemaker or implantable heart defibrillator, a history of bleeding problems, dilated blood vessels, and any other previously known problems with your esophagus.


Seven days before the monitoring period, do not take proton pump inhibitors such as omeprazole (Prilosec®), lansoprazole (Prevacid®), rabeprazole (Aciphex®), pantoprazole (Protonix®), esomeprazole (Nexium®).

Two days (48 hours) before the monitoring period, do not take the H2 blockers ranitidine (Zantac®), cimetidine (Tagamet®), famotidine (Pepcid®), nizatidine (Axid®); or the promotility drug, metoclopramide (Reglan®).

Six hours before the monitoring period, do not take antacids (such as Alka-Seltzer®, Gaviscon®, Maalox®, Milk of Magnesia®, Mylanta®, Phillips®, Riopan®, Tums® or any other brands).

Four to 6 hours before your appointment do not eat or drink.

Please note: Occasionally, your doctor may want you to continue taking a certain medication during the monitoring period to determine if it is effective.




Once the test has begun, what do I need to know and do?

Activity: Follow your usual daily routine. Do not reduce or change your activities during the monitoring period. Doing so can make the monitoring results less useful. Note: Do not get the receiver wet; it is not waterproof!

Eating: Eat your regular meals at the usual times. If you do not eat during the monitoring period, your stomach will not produce acid as usual, and the test results will not be accurate. Eat at least 2 meals a day. Eat foods that tend to increase your symptoms (without making yourself miserable). Avoid snacking. Do not suck on hard candy or lozenges and do not chew gum during the monitoring period.
Lying down: Remain upright throughout the day. Do not lie down until you go to bed (unless napping or lying down during the day is part of your daily routine).

Medications: Continue to follow your doctor’s advice regarding medications to avoid during the monitoring period.

Recording symptoms: Press the appropriate button on the receiver when symptoms occur (as discussed with the nurse). Record the time you start and stop eating and drinking (anything other than plain water). Record the time you lie down (even if just resting) and when you get back up. The nurse will explain this.

Unusual symptoms or side effects: If you think you may be experiencing any unusual symptoms or side effects, call your doctor.
You will return the receiver and diary when the monitoring period is over. The information on the receiver and diary will be downloaded to a computer and the results will be analyzed. Preliminary study data will be reviewed with you if you desire.




After completion of the study:

Resume your normal diet and medications.

Your doctor will discuss the results of your test with you during your next scheduled appointment.

Normal activities – such as swallowing, eating and drinking – will cause the disposable pH capsule to detach and pass through the digestive tract in 7 to 10 days on average.

No MRI exams (magnetic resonance imaging) should be performed for 30 days following capsule insertion."

These are the five main tests that are preformed to properly diagnose Gastroparesis. Doctors may use a combination of these tests to determine if:

1. You have Gastroparesis
2. How mild to severe your Gastroparesis is

I did not really get into endoscopies and upper GI testing, like barium swallows, because those are not the best tests to determine whether or not someone has Gastroparesis. These tests can definitely be useful, and I am not debating that, but there are a lot of things that can missed on tests like these. My GI did an endoscopy on me, before he hospitalized me to do more testing (before I even knew what Gastroparesis was) and when I came to, he started getting on to me about eating after midnight and not telling them. I swore to him that I had not eaten or had anything to drink after midnight. I told him the last thing I ate, which was three days before the endoscopy, was a salad. He was appalled because I still had undigested salad greens sitting in my stomach. After that, he hospitalized me and did a gastric emptying study. At the end of the day, endoscopies and barium swallows can help confirm a diagnosis, but the other tests are a lot more accurate in diagnosing Gastroparesis, in my opinion, but you should talk with your doctor about the different test options if you suspect that you have Gastroparesis, or if a family member does.

The Many Causes of Gastroparesis & Treatment Options

Gastroparesis can be caused by many things. My Gastroparesis is Idiopathic, according to the US National Library of Medicine National Institutes of Health, it means, "delayed gastric emptying can be due to muscular, neural, or humoral abnormalities. In the absence of an identified cause, gastroparesis is labelled as Idiopathic." I suspect I have had it since I was sixteen. I became really sick and was running a high fever, so my mom took me to the Emergency Room. I was admitted and taken for emergency surgery because my GI thought I had appendicitis. When they went in for abdominal surgery, the doctor found that my appendix was fine. Furthermore, I had ovarian cysts that had ruptured, and the fluid was sitting in my abdomen causing a bad infection. The doctors cleaned out my abdomen, but took my appendix anyway. I have been vomiting since then.

I decided to do an article exploring what causes Gastroparesis. I have been asked this a lot by newly diagnosed Gastroparesis Warriors, and I was curious to see if anything has changed, especially given all of the awareness to this illness that the wonderful members of the GP Community have dedicated themselves to in the past few years. I also wanted to have an article written about what causes Gastroparesis, so that people who are having symptoms of this illness, can have something to refer back to so that the doctor will know what tests to run. If you think you might have Gastroparesis, definitely talk to your Gastroenterologist.



I keep a journal, like so:

Your journal could be a spiral notebook, a binder, a lab notebook, just anything, really. I have two separate ones.

I write down any questions I have for the doctor, and print out research, to put it in the journal and ask the doctor about it. Finally, I ask questions in support groups and write down the answers I get, or print them out and stick them in my journal. Furthermore, if I think a question is interesting that someone else posted, I will print out that posting with the questions and places them in my blog to talk to the doctor about, as well. You can put your medication times, what you take, and how often in there to keep up with things. Additionally, you can write about your diet; what you have eaten, how many servings you had, calories, fiber (since with GP it is hard to digest fiber), and food allergies. If you get sick, put how many times you got sick, and what the time was. You might be able to see a pattern that can be graphed and followed.





What is Gastroparesis?

This is a video, uploaded by a doctor, that will explain Gastroparesis, but also contains graphic images during an exploratory abdominal surgery (this is warning to those of you who are squeamish): https://www.youtube.com/watch?v=v-yeVxI4CeE

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According to Active Beat,

"Gastroparesis is the literal paralysis of the stomach, characterized as a condition that inhibits the stomach from emptying properly. Gastroparesis affects stomach contractions, which move food from the stomach into the large intestine where digested food is emptied. If stomach contractions don’t work to empty the stomach properly, gastro-discomfort can occur (i.e., nausea, bloating, vomiting) and individuals can suffer nutritional deficiencies as a result.

Here are six common causes and symptoms that accompany Gastroparesis:


Existing Medical Conditions

The most common causes linked to Gastroparesis include existing health conditions, such as a viral infection, eating disorder, cancer with radiation and/or chemotherapy, and gastric surgery (or stomach surgery) that causes vagus nerve damage. Specific medications can also trigger gastroparesis (i.e., progesterone, lithium, antidepressants, clonidine, and calcium channel blockers). Use of nicotine, especially smoking over the long term is also common in gastroparesis patients.

Certain chronic diseases—such as uncontrolled diabetes, hypothyroidism, multiple sclerosis, and Parkinson’s disease—have also been associated with the development of gastroparesis. Rare conditions that impact the functioning of connective tissues, blood vessels, skin, muscles, and internal organs (i.e., scleroderma and amyloidosis) have also been linked to causing digestive stomach issues.

Source: https://www.researchgate.net/figure/Pathophysiology-of-Idopathic-Gastroparesis_fig1_316506590



Doctors often have issue pinpointing the exact cause of Gastroparesis. Diagnosis with unknown cause is common and known as Idiopathic Gastroparesis by health professionals.

Even though the cause of idiopathic gastroparesis remains unknown, researchers the Mayo Clinic claim that women ranging from young to middle aged are at highest risk of developing idiopathic gastroparesis.

Image Source: Located Above





According to the US National Library of Medicine and National Institutes of Health,

"Gastroparesis is a chronic symptomatic disorder of the stomach characterized by delayed emptying without evidence of mechanical obstruction. The main causes of gastroparesis are diabetic, postsurgical, and idiopathic. Idiopathic gastroparesis refers to gastroparesis of unknown cause, that is, not from diabetes, not from prior gastric surgery, and not related to other endocrine, neurologic, rheumatologic causes of gastroparesis. The gastroparesis should not be related to medications that can delay gastric emptying, such as narcotic analgesic or anticholinergic medications. There is overlap in the symptoms of idiopathic gastroparesis and functional dyspepsia. A substantial minority of patients with functional dyspepsia can have delayed gastric emptying, blurring the distinction between idiopathic gastroparesis and functional dyspepsia. Patients with idiopathic gastroparesis often have a constellation of symptoms including nausea, vomiting, early satiety, postprandial fullness, and upper abdominal pain. Although the presentation of idiopathic gastroparesis is relatively similar to diabetic gastroparesis, abdominal pain occurs more often in idiopathic gastroparesis, whereas nausea and vomiting are more severe in diabetic gastroparesis. Treatment may employ agents used for diabetic gastroparesis and functional dyspepsia, including dietary management, prokinetics agents, antiemetic agents, and symptom modulators. Current treatment options do not adequately address clinical need for idiopathic gastroparesis.



Gastroparesis is a chronic symptomatic disorder of the stomach manifested by delayed emptying without evidence of mechanical obstruction (1,2). The common causes of gastroparesis include diabetic, postsurgical, and idiopathic (1,2). Idiopathic gastroparesis refers to gastroparesis of unknown cause; that is, not from diabetes, not from prior gastric surgery, and not related to other endocrine, neurologic, rheumatologic causes of gastroparesis. In addition, it is not related to medications that can delay gastric emptying. Medications known to delay gastric emptying include opiate narcotic analgesics and anticholinergics (1).

In most series, idiopathic gastroparesis is the most common category for gastroparesis. In the series reported by McCallum et al (3), the etiologies in 146 patients were: 36% idiopathic, 29% diabetic, and 13% postgastric surgery, 7.5% Parkinson’s disease, 4.8% collagen vascular disorders, 4.1% intestinal pseudoobstruction, and 6% miscellaneous causes. Miscellaneous causes of gastroparesis include other neurologic diseases, eating disorders, other metabolic or endocrine conditions (hypothyroidism), and critical illness.

This chapter discusses idiopathic gastroparesis, that is, symptomatic gastroparesis not from other known etiologies. This chapter updates the present status of our understanding of this disorder and reviews the recent studies from the NIH NIDDK Gastroparesis Consortium.




Epidemiology

Gastroparesis occurs more often in women than men, often by a 3:1 margin. Interestingly, this is true not only for idiopathic gastroparesis, but also for the other main causes of gastroparesis - diabetic and postsurgical. Patients with idiopathic gastroparesis are typically young or middle-aged women. Even after adjusting for gender differences in gastric emptying, since females in general have slower gastric emptying than males (4), gastroparesis occurs more commonly in women (5).

Outside of gender issues and etiology, the epidemiology of gastroparesis has not been well systematically studied. This stems from the fact that for proper diagnosis, a gastric emptying test is needed; one that presently cannot be done in population studies. Data from the Rochester Epidemiology Project, a database of linked medical records of residents of Olmsted County, Minnesota, showed that the age-adjusted incidence of definite gastroparesis per 100,000 person-years for the years 1996 to 2006 was 9.8 for women and 2.4 for men (6). Definite gastroparesis was defined as diagnosis of delayed gastric emptying by standard scintigraphy and symptoms of nausea and/or vomiting, postprandial fullness, early satiety, bloating, or epigastric pain for more than 3 months. The age-adjusted prevalence of definite gastroparesis per 100,000 persons was 37.8 for women and 9.6 for men. More recent estimates have suggested that the prevalence of gastroparesis were an underestimation and the prevalence is greater, approaching 2% of the general population (7).






Symptoms

Common symptoms of gastroparesis include nausea (>90% of patients), vomiting (84% of patients), and early satiety (60% of patients) (1,2,3). Other symptoms include postprandial fullness and upper abdominal pain (8). There is slight variation in symptoms depending on the etiology of gastroparesis: abdominal pain occurs more often in idiopathic gastroparesis than in diabetic gastroparesis (8), whereas nausea and vomiting are more severe in diabetic gastroparesis then in idiopathic gastroparesis (9). In patients with gastroparesis, weight loss, malnutrition, and dehydration may be prominent in severe cases.

There is overlap in the symptoms of idiopathic gastroparesis and functional dyspepsia. Abdominal pain or discomfort may be present to varying degrees in patients with gastroparesis, but it is not usually the predominant symptom, as it can be in functional dyspepsia (10). A substantial minority of patients (20–40%) with functional dyspepsia can have delayed gastric emptying (10), blurring the distinction between idiopathic gastroparesis and functional dyspepsia. Patients with idiopathic gastroparesis often have a constellation of symptoms including nausea, vomiting, early satiety, postprandial fullness, and upper abdominal pain.

Symptoms may fluctuate, with episodes of pronounced symptoms interspersed with relatively symptom-free intervals. Thus, at times, it can be difficult to differentiate idiopathic gastroparesis from cyclic vomiting syndrome (CVS), especially in the later when there can be a “coalescence of symptoms”, such that they can occur nearly daily rather than as typical for CVS with the vomiting episodes more sporadic on a monthly or less frequent basis (11). In CVS, gastric emptying is normal or often, it can be rapid (11)

The symptom profile and symptom severity of gastroparesis can be assessed with the Gastroparesis Cardinal Symptom Index (GCSI) (12), a subset of the Patient Assessment of Upper Gastrointestinal Symptoms (PAGI-SYM) (13). The GCSI comprises 3 subscales (nausea and vomiting, postprandial fullness and early satiety, and bloating) that the patient scores with reference to the preceding 2 weeks (12). The GCSI daily diary (GCSI-DD) can be used to record symptoms on a daily basis and may be more accurate in recording symptoms (14). This daily diary of symptoms captures symptoms of early satiety, nausea, vomiting, postprandial fullness, and upper abdominal pain. This questionnaire has been shown to capture relevant symptoms of gastroparesis in both patients with diabetic gastroparesis and idiopathic gastroparesis.

Although it has been a common assumption that the gastrointestinal symptoms can be attributed to the delay in gastric emptying characteristic of the disorder, most investigations have observed only weak correlations between symptom severity and the degree of gastric stasis (15,16). In general, the symptoms that appear to be best correlated (significant, but low correlation coefficients of 0.2 to 0.3) with a delay in gastric emptying include nausea, vomiting, early satiety, and postprandial fullness (17,18). Some symptoms present in patients with gastroparesis such as bloating and upper abdominal pain, are not correlated with delayed gastric emptying and might be related to sensory alterations that might also be present in patients with gastroparesis (18).

Most gastroparetic patients are underweight probably because of frequently experienced early satiety, nausea, and vomiting. Some gastroparesis (GP) patients, however, are overweight, for reasons that are not well understood. In a recent study, the factors that influence bodyweight in patients with idiopathic GP and in healthy controls were investigated (19). Thirty-nine healthy controls and 29 subjects with idiopathic GP underwent resting energy expenditure (indirect calorimetry), body composition (bioelectrical impedance), dietary intake (Block Food Frequency Questionnaire), symptoms (Patient Assessment of Upper GI Symptoms), and physical activity (Paffenbarger exercise survey) were assessed. Both median caloric intake (1242 vs 1804 kcal; p=0.005) and caloric expenditure (486 vs 2172 kcal; p<0 .01="" 0.05="" 1134="" 12="" 1422="" 17="" 19.3="" 24.3="" 243="" 41="" 644="" a="" abdominal="" activity="" addressed="" age="" although="" an="" and="" as="" at="" because="" bmi="" caloric="" calories="" center="" centers="" characteristics="" clinical="" common="" compared="" consortium="" consumed="" controls.="" controls="" cooperative="" coordinating="" data="" delay="" described="" diabetes="" diagnosis="" digestive="" diseases="" emptying="" energy="" enrolled="" expended="" expenditure.="" expenditure="" female.="" for="" funded="" gained="" gastric="" gastroparesis.="" gastroparesis="" gp="" gpc="" gpcrc="" had="" have="" health="" healthy="" idiopathic="" implemented="" in="" increased="" institute="" institutes="" intake="" interestingly="" is="" kcal="" kg="" kidney="" largest="" less="" lost="" lower="" m2="" majority="" mean="" median="" more="" most="" national="" nausea="" network="" neutral.="" niddk="" nih="" observational="" of="" one="" or="" p="0.45)" pain="" patients="" pcrc="" per="" presenting="" prospectively="" published="" recently="" reduced="" registry="" remained="" research="" resting="" seven="" several="" severe="" severity="" significantly="" similar.="" since="" studies="" study="" subgroup="" symptom="" symptomatic="" symptoms="" than="" the="" this="" through="" thus="" to="" vomiting="" vs="" was="" week="" weight="" were="" who="" with="" years="">35% retention at 4 hours) was present in 28% of patients and was associated with more severe symptoms of nausea and vomiting and loss of appetite compared with patients with mild or moderate delay. Of these patients with idiopathic gastroparesis, 86% met criteria for functional dyspepsia, predominately postprandial distress syndrome. Of interest, 46% of the patients were overweight. Thus, this study shows that idiopathic gastroparesis is a heterogeneous syndrome that primarily affects young women and can also affect overweight or obese individuals.

Although gastroparesis can be diabetic or idiopathic, little is known about differences in their presentation. The GpC compared clinical characteristics, symptoms, and gastric emptying in patients with idiopathic gastroparesis (IG) to patients with type 1 or type 2 diabetic (DG) (21). 416 patients with gastroparesis were analyzed; 254 had IG, and 137 had DG (78 had type 1 and 59 had type 2). Symptoms that prompted evaluation more often included vomiting for DG and abdominal pain for IG. Patients with DG had more severe retching and vomiting than those with IG, whereas patients with IG had more severe early satiety and postprandial fullness subscores. Compared with IG, gastric retention was greater in patients with type 1 DM. Thus, there are many similarities and some differences in clinical characteristics of DG and IG. Gastroparesis is a heterogeneous disorder; the etiology of the gastroparesis impacts on the symptoms and severity.

Abdominal pain can be present in patients with idiopathic gastroparesis. Factors associated with abdominal pain in gastroparesis have not been well studied. The NIH GpC studied the symptom of abdominal pain and how it relates to other clinical factors in 393 gastroparesis patients (22). Upper abdominal pain was moderate-severe in 261 (66%) patients. Pain/discomfort was predominant in 81 (21%); nausea/vomiting was predominant in 172 (44%). Moderate-severe pain was more prevalent with idiopathic gastroparesis than in diabetic gastroparesis and correlated with scores for nausea/vomiting and opiate use, but not gastric emptying. Gastroparesis severity, quality of life, and depression and anxiety were worse with moderate-severe pain. Predominant pain/discomfort was associated with impaired quality of life. Thus, moderate-severe abdominal pain is prevalent in gastroparesis, impairs quality of life, and is associated with idiopathic etiology, and opiate use. Pain was predominant in one fifth of gastroparetics. Predominant pain has at least as great an impact on disease severity and quality of life as compared to the more classic symptoms of predominant nausea/vomiting.

Bloating is commonly reported in gastroparesis, but is an underappreciated symptom of gastroparesis. The prevalence of bloating in gastroparesis and its severity was assessed in 335 gastroparesis patients (23). Bloating severity of at least severe (GCSI ≥4) grades was reported by 41% of patients. Bloating severity related to female gender and overweight status and correlated with intensity of nausea, postprandial fullness, visible distention, abdominal pain, and altered bowel function. Antiemetics, probiotics, and antidepressants with significant norepinephrine reuptake inhibitor activity may affect reports of bloating. Disease-specific quality of life and general measures of well-being were progressively impaired with increasing bloating severity. Thus, the symptom of bloating impairs quality of life but is not influenced by gastric emptying rates.

Many patients with gastroparesis have had their gallbladders removed; how this impacts on gastroparesis is not known. The clinical presentations of patients with gastroparesis were compared in those with prior cholecystectomy compared to patients who have not had their gallbladder removed (24). Of 391 subjects with diabetic or idiopathic gastroparesis (IG), 142 (36 %) had a prior cholecystectomy. Patients with prior cholecystectomy were more often female, older, and overweight or obese. Cholecystectomy had been performed in 46% of T2DM compared to 24% of T1DM and 38% of IG. Patients with cholecystectomy had more comorbidities, particularly chronic fatigue syndrome, fibromyalgia, depression, and anxiety. Postcholecystectomy gastroparesis patients had increased health care utilization, and had a worse quality of life. Etiology was not independently associated with a prior cholecystectomy. Thus, symptom profiles in patients with and without cholecystectomy differ: postcholecystectomy gastroparesis patients had more severe upper abdominal pain and retching and less severe constipation. These data

Source: Located on Image






Pathophysiology

A potential cause in some patients with idiopathic gastroparesis has been suggested to be viral injury to the nerves or muscles of the stomach – postviral gastroparesis. It has been suggested that idiopathic gastroparesis of acute onset with infectious prodrome could constitute postviral or viral injury to the neural innervation of the stomach or the interstitial cells of Cajal in the stomach. In the NIH GpC study of idiopathic gastroparesis, half the patients had an acute onset of symptoms with a minority of patients (19%) reported an initial infectious prodrome such as gastroenteritis or respiratory infection (20). In the McCallum series, postviral gastroparesis was suspected in 23% of patients with idiopathic gastroparesis (25). This clinical diagnosis of postviral gastroparesis is suggested in previously healthy persons with an acute onset of viral illness with nausea, vomiting, diarrhea, fever, and cramps who have persistence of symptoms (nausea, vomiting, early satiety) for more than 3 months with a delay in gastric emptying. Viruses suspected as potential causes are cytomegalovirus (CMV), Epstein–Barr virus, and herpes varicella-zoster. Symptoms of idiopathic gastroparesis after a presumed viral illness tend to be less severe than in gastroparesis from other causes. Overall, these patients appear to have a good prognosis, with many patients having a slow resolution of their symptoms (25).

Gastric emptying is mediated by the vagus nerve, which helps regulates fundic accommodation, antral contraction, and pyloric relaxation (1). These regional gastric motility changes with food ingestion are then mediated through smooth muscle cells, which control stomach contractions; interstitial cells of Cajal, which regulate gastric pacemaker activity; and enteric neurons, which initiate smooth muscle cell activity (1). The pathophysiology of gastroparesis has not been fully elucidated but appears to involve abnormalities in functioning of several elements including autonomic nervous system, smooth muscle cells, enteric neurons, and interstitial cells of Cajal. Histologic studies in gastroparesis patients demonstrate defects in the morphology of enteric neurons, smooth muscle cells, and interstitial cells of Cajal and increased concentrations of inflammatory cells in gastric tissue (26).

NIH Gastroparesis Consortium Studies on Pathology
Cellular changes associated with diabetic (DG) and idiopathic gastroparesis (IG) have recently been described from gastroparesis patients by the NIH GpC. Full-thickness gastric body biopsy specimens were obtained from 40 patients with gastroparesis (20 diabetic) and matched controls (27). Histologic abnormalities were found in 83% of patients. The most common defects were loss of ICC with remaining ICC showing injury, an abnormal immune infiltrate containing macrophages, and decreased nerve fibers. On light microscopy, no significant differences were found between diabetic and idiopathic gastroparesis with the exception of nNOS expression, which was decreased in more patients with idiopathic gastroparesis (40%) compared with diabetic patients (20%) by visual grading. On electron microscopy, a markedly increased connective tissue stroma was present in both disorders. This study suggests that on full-thickness biopsy specimens, cellular abnormalities are found in the majority of patients with gastroparesis. The most common findings were loss of Kit expression, suggesting loss of ICC, and an increase in CD45 and CD68 immunoreactivity. These findings suggest that examination of tissue can lead to valuable insights into the pathophysiology and possibly treatments for the patient.

The association of these cellular changes in patients with gastroparesis with gastroparesis symptoms and gastric emptying was recently reported (28). Idiopathic gastroparesis with a myenteric immune infiltrate scored higher on the average GCSI and nausea score as compared to those without an infiltrate. Interstitial cells of Cajal counts inversely correlated with 4 h gastric retention in DG but not in IG. There was also a significant correlation between loss of ICC and enteric nerves in DG but not in IG. Thus, in DG, loss of ICC is associated with delayed gastric emptying. Interstitial cells of Cajal or enteric nerve loss did not correlate with symptom severity. Overall clinical severity and nausea in IG is associated with a myenteric immune infiltrate. Thus, full thickness gastric biopsies can help define specific cellular abnormalities in gastroparesis, some of which are associated with physiological and clinical characteristics of gastroparesis.




Management

Management of gastroparesis is guided by the goals of correcting fluid, electrolyte, and nutritional deficiencies; identifying and treating the cause of delayed gastric emptying (e.g., diabetes); and suppressing or eliminating symptoms (1,2). Treatment of the symptoms may employ agents used for diabetic gastroparesis and functional dyspepsia. Care of patients generally relies on dietary modification, prokinetics medications that stimulate gastric motor activity, antiemetic drug therapy to suppress symptoms of nausea and vomiting, and symptom modulators (psychotropic agents) that reduce symptom expression. Narcotic analgesics should be avoided. Although narcotic analgesics may acutely improve abdominal pain, with chronic use, they delay gastric emptying, may themselves lead to symptoms of nausea and vomiting, may upregulate abdominal pain, and lead to dependence. Total parenteral nutrition, although used in some refractory patients, is associated with complications of infections and thrombosis. Aspects on treatment are discussed in detail in later chapters on treatments for gastroparesis. Particulars of treatment in idiopathic gastroparesis are discussed below.




Dietary aspects in gastroparesis

Gastroparesis can lead to food aversion, poor oral intake, and subsequent malnutrition. In the NIH GPC gastroparesis registry, dietary intake and nutritional deficiencies were characterized in 305 patients with diabetic and idiopathic gastroparesis (29) who completed diet questionnaires (Block Food Frequency Questionnaire). Caloric intake averaged 1168±801 kcal/day, amounting to 58%±39% of daily total energy requirements (TER). A total of 194 patients (64%) reported caloric-deficient diets. Only 5 patients (2%) followed a diet suggested for patients with gastroparesis. Deficiencies were present in several vitamins and minerals; patients with idiopathic disorders were more likely to have diets with estimated deficiencies in vitamins A, B6, C, K, iron, potassium, and zinc than diabetic patients. Only one-third of patients were taking multivitamin supplements. More severe symptoms (bloating and constipation) were characteristic of patients who reported an energy-deficient diet. Surprisingly, only 32% of patients had nutritional consultation after the onset of gastroparesis; consultation was more likely among patients with longer duration of symptoms and more hospitalizations and patients with diabetes. Multivariable logistic regression analysis indicated that nutritional consultation increased the chances that daily TER were met (odds ratio, 1.51; P=0.08). Thus, many patients with gastroparesis have diets deficient in calories, vitamins, and minerals. Most patients are not following a “gastroparesis diet”. Nutritional consultation is obtained infrequently, especially in idiopathic gastroparesis. A nutritional consultation may be helpful for instructions on dietary therapy and to address nutritional deficiencies.

Source: Located on Image

Source: Located on Image


I also have information on my blog regarding the Gastroparesis Diet, including recipes and links to more recipes: http://www.emilysstomach.com/2014/01/the-gastroparesis-diet.html





Psychotropic medications as symptom modulators

Gastroparesis is a challenging syndrome to manage, with few effective treatments and lack of rigorously controlled trials. Symptom modulators (psychotropic agents such as tricyclic antidepressants) are often used to treat refractory symptoms of nausea, vomiting, and abdominal pain. Evidence from well-designed studies for this use is lacking. Tricyclic antidepressants may have benefits in suppressing symptoms in some patients with nausea and vomiting as well as patients with abdominal pain. Doses of tricyclic antidepressants used are lower than used to treat depression. A reasonable starting dose for a tricyclic drug is 10–25 mg at bedtime. If benefit is not observed in several weeks, doses are increased by 10- to 25-mg increments up to 75 mg. Side effects are common with use of tricyclic antidepressants and can interfere with management and lead to a change in medication in some patients. The secondary amines, nortriptyline and desipramine, may have fewer side effects than amitriptyline which itself may delay gastric emptying. The recent NIH gastroparesis consortium study with nortriptyline in idiopathic gastroparesis did not show an effect on overall symptoms of gastroparesis (30). However, there was a suggestion that low nortriptyline doses (10–25 mg qhs) might decrease nausea, whereas higher doses might decrease fullness. The recently completed NIH functional dyspepsia treatment trial showed a favorable effect for amitriptyline for functional dyspepsia – this was seen in patients with normal gastric emptying, but not in those with delayed gastric emptying (31).




Gastric electric stimulation

Gastric electric stimulation is a treatment for refractory gastroparesis involving implantation of neurostimulator. The currently approved stimulator delivers a high-frequency (12 cpm), low-energy signal with short pulses to the gastric muscle along the greater curvature. Based on the initial studies that have shown symptom benefit with low complications, the gastric electric neurostimulator was granted humanitarian approval from the FDA for the treatment of chronic, refractory nausea and vomiting secondary to idiopathic or diabetic gastroparesis (32). Symptoms of vomiting improved with gastric stimulation. This symptomatic benefit was primarily seen in patients with diabetic gastroparesis than in idiopathic gastroparesis (32). In the study by Maranki et al (33), three predictive factors for clinical improvement with gastric electric stimulation were found: 1) diabetic rather than idiopathic etiology; 2) predominant symptoms of nausea and/or vomiting rather than abdominal pain; 3) lack of the use of regular narcotic pain medications. In this series, gastric electric stimulation significantly improved symptoms of nausea and vomiting, but not abdominal pain. In a recently reported, prospective study of gastric electric stimulation for idiopathic gastroparesis (34), there was a reduction in vomiting during the initial 6 week open label ON treatment period. A double-blind 3-month period showed a non-significant reduction in vomiting in the ON vs OFF period, the primary outcome variable. At 12 months with open label ON stimulation, there was a sustained decrease in vomiting and days of hospitalizations.

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Conclusions

Idiopathic gastroparesis refers to gastroparesis of unknown cause, that is, not from diabetes, not from prior gastric surgery, and not related to other endocrine, neurologic, rheumatologic causes of gastroparesis. Patients with idiopathic gastroparesis often have a constellation of symptoms including nausea, vomiting, early satiety, postprandial fullness, and upper abdominal pain. Although the presentation of idiopathic gastroparesis is relatively similar to diabetic gastroparesis, abdominal pain occurs more often in idiopathic gastroparesis, whereas nausea and vomiting are more severe in diabetic gastroparesis. Treatment may employ agents used for diabetic gastroparesis and functional dyspepsia, including dietary management, prokinetics agents, antiemetic agents, and symptom modulators. Idiopathic gastroparesis significantly impacts on the quality of life of patients through its chronic symptoms of nausea, vomiting, and abdominal pain. Unfortunately, current approved treatment options do not adequately address clinical need. Development of new effective therapies for symptomatic control is needed.




​
Key Points

Idiopathic gastroparesis is a common form of gastroparesis, being among the three main causes of gastroparesis: diabetic, postsurgical, and idiopathic gastroparesis.

Patients with idiopathic gastroparesis has a constellation of symptoms including nausea, vomiting, early satiety, postprandial fullness, and, in some patients, upper abdominal pain.

The presentation of idiopathic gastroparesis is relatively similar to diabetic gastroparesis, although abdominal pain occurs more often in idiopathic gastroparesis, whereas nausea and vomiting are more severe in diabetic gastroparesis.

Treatment of the symptoms may employ agents used for diabetic gastroparesis and functional dyspepsia.
Idiopathic gastroparesis significantly impacts on the quality of life of patients and development of new effective therapies for symptomatic control is needed.



Footnotes

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Source: Imgur (Digestive Health Center for both images)








I found a wonderful slide show, by Lazoi Lifecare Private Limited, which explains what can cause Gastroparesis:

According to the Cleveland Clinic,

"A look at what causes gastroparesis



The primary cause of gastroparesis is damage to or dysfunction of peripheral nerves and muscles.



In diabetic patients, Dr. Cline says, it appears as more of a neuropathy-based disease associated with damaged nerves. In patients who don’t have diabetes, it seems more muscular-based: The nerve endings are all right, but the muscles are not responding, he says.



In addition to diabetes, other sources of gastroparesis include:


Lingering post-viral effects — You get a virus, but the nausea and vomiting from the virus don’t go away after the virus is gone.'Some of those cases will resolve, and we just have to wait and watch,' Dr. Cline says. 'But a lot of times it doesn’t resolve, so we have to continue to treat the patients.'

Connective tissue diseases — Gastroparesis may plague patients who have diseases such as multiple sclerosis or muscular dystrophy.

Side effects from medication — Probably the most difficult group to treat, narcotic pain medicines and other drugs slow a patient’s intestinal motility, Dr. Cline says. 'That can be very hard to treat, because the medications often override what we prescribe to treat the gastroparesis.'

Post-surgical effects — Some patients develop gastroparesis after the vagus nerve is damaged or trapped during a gastrointestinal surgical procedure.






A difficult disease to treat



Treatment sometimes begins with adjustments to diet and medication. If those approaches don’t work, surgical treatments are the next steps:


Feeding tube — Because gastroparesis impairs proper nutrition, surgeons can insert a feeding tube through the patient’s nose that bypasses the stomach. Or a surgeon may place what is known as a J tube directly into the patient’s small bowel for feeding.If these don’t work, total patient nutrition (TPN) is the next step. The patient is fed through an IV.


Gastric pacemaker — A surgeon also may use a minimally invasive laparoscopic procedure to implant a gastric pacemaker to treat this chronic digestive condition.The small device employs gentle electrical impulses to stimulate the stomach’s muscles to perform their usual functions. 'These impulses help move the stomach’s contents through the digestive tract and bring the patient relief from symptoms. We’re moving towards not really curing gastroparesis — because we really don’t know how to reverse the neuropathies yet — but fixing it as best we can,' says Dr. Cline. 'So patients and their families need to push for the diagnostic tests that we can do, because the earlier it’s diagnosed, the easier it is to treat.'

Source: Imgur






Treating Psychological Concerns


A neuropsychiatric specialist is sometimes called in to address mental health concerns that can accompany this chronic disease.


'If you wake up sick every day and vomiting all the time, this disease can quickly move from a purely physical one to a psychiatric one, so we treat the possible components of depression, anxiety, pain and so on, too,' Dr. Cline says.

I am currently working on an article about the different feeding tubes and going into researched detail about all of them, which will be ready soon. I wanted to do some research into them, because I know most of the questions I get are about feeding tubes. I, personally, do not have a feeding tube yet, but I am going to ask my doctor about treatment options because I do vomit a lot. While I do not think it's all psychological, I do think anxiety makes it worse. How could you not be anxious knowing you are in a vomiting cycle?

If you were told recently that you need one, I will try to get it ready faster, so that you can look over it. However, it's always good to do your own research as well, and really think about what questions to write down that you can ask the doctor.



I hope this will help for now:

Source: Located on Image

Source: https://goo.gl/images/K4MwoH