Friday, August 24, 2007

Gastroparesis meds- what do you use?

Posted by cj on August 12, 2007 at 02:44:07:
In Reply to: gastroparesis meds- what do you use? posted by judylu on August 12, 2007 at 01:00:18:


Jerry took reglan, propulsid. none worked like this:::: erythromyacin liquid. 1/8th teaspoon before meals. the side effects of this antibiotic they have found will cause motility (cramping)but very mild,since you are using it theraputically , not as an antibiotic.

NOW youll be hard pressed to find any info on gastroparesis that doesnt involve diabetes. it doesnt matter because the symptoms/treatments are the same. It is all damage to the vagus nerve.
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Gastroparesis doesn't sound good, and it isn't. Literally "stomach paralysis," it is a form of diabetic neuropathy, or nerve damage, that is a common complication of diabetes. The damaged nerve in question is the vagus nerve, named for its vagabond-like wandering nature.

The vagus nerve meanders all the way from the brainstem to the colon, controlling heart rate, sweating, gastrointestinal contractions, and various other involuntary, automatic functions on its way. In the case of gastroparesis, it's the vagus nerve's control of stomach contractions that's damaged.

The stomach is basically a hollow ball made of muscle that serves as a storage container and mixing bowl for food. It's about the size of a small melon, but it can stretch to hold nearly a gallon if you really press the issue. In healthy people, wave-like contractions of the stomach, prompted by the vagus nerve, crush and churn your food into small particles and mix it up with enzymes and acids produced by the stomach's inner lining.

Then the stomach contractions, coming along in waves at about three per minute, slowly and evenly propel the pulverized food out through the pyloric valve, which opens just enough to release an eighth of an ounce of food at a time. From there it's down the small intestine, where the real nutrient absorption occurs. It can take four hours to empty your stomach into your small intestine, especially if you've eaten fat, which slows the process down.

If the vagus nerve has been damaged by years of high blood sugars, the process hits a snag. The walls of the stomach, paralyzed by the lack of vagus nerve stimulation, don't make their muscular wave-like contractions. As a result, food just sticks around in the stomach, unpulverized and going nowhere. It may sit and ferment, creating an environment that fosters the growth of harmful bacteria.

Alternatively, the food can harden into solid masses called bezoars (pronounced "bee's oars") that are similar to a cat's hairball. In olden days, bezoars were thought to be magical poison antidotes and were worth several times their weight in gold. These days, however, all they do is cause nausea and vomiting. Worst case scenario, they can even block the pyloric valve, creating a serious emergency.

The common symptoms of gastroparesis are bloating, abdominal pain, nausea, feeling full after just a few bites of a meal, weight loss, and heartburn. Nausea and vomiting generally occur many hours after the last meal, usually when your stomach is fullest from both food and the secretions stimulated by the food. Because the food hasn't been ground up during the interim, it often comes up in the same shape it went down in, so it is, unpleasantly enough, easily recognized.

Diabetes is the leading risk factor for gastroparesis. About one in five people with type 1 develop it, as well as many people with type 2. Once it develops, it makes blood sugar management even harder because erratic stomach emptying make blood sugar levels difficult to predict and control. Conversely, poor control of blood sugar levels makes gastroparesis worse by tending to slow gastric emptying.

There are any number of new methods to look for gastroparesis, many of which involve eating or drinking something rather unappetizing. In a gastric emptying study, considered one of the most accurate methods to diagnose gastroparesis, you must eat eggs or oatmeal containing a harmless radioactive substance that makes the food visible on a Geiger-counter-like scan. Less commonly, you might undergo a barium x-ray, in which you fast for twelve hours and then drink a sludgy liquid that coats the inside of your stomach and makes its contents visible on x-ray.

Other diagnostic tests involve threading a little tube down into your stomach to assess the strength, frequency, and coordination of your stomach contractions or the electrical signals that travel through your stomach and stimulate its contractions.

The simplest way to address gastroparesis is through dietary changes. Smaller, more frequent meals ameliorate that feeling of fullness and are faster and easier to digest than three big meals. If your appetite diminishes later in the day, eat more in the morning and stick to liquids in the afternoon. By lying on your right side after eating, you can put gravity to work to help empty your stomach.

A big problem is fiber, which helps things move along in the intestines but has the opposite effect in the stomach. The stomach has a hard time breaking down roughage, which is also more likely to sit around and form those unwanted bezoars. So people with gastroparesis are often advised to avoid raw vegetables and eat soft, low-fiber foods like well-cooked fruits and vegetables, fish, chicken, yogurt, refined breads and grains, or pureed or liquid foods.

Sometimes it's advisable to avoid fats, which slow down stomach emptying even in healthy people. If you're vomiting a lot, it's also important to drink water to avoid dehydration and to take supplements in liquid form. If you can't tolerate any food or liquid at all, your doctor might place a feeding tube in your small intestine to bypass your stomach altogether. It's usually a temporary fix, used only in severe cases or when blood sugar levels can't be controlled.

Sometimes gastroparesis can be worsened, or even caused, by medications that slow stomach emptying, including narcotic pain medications, tricyclic anti-depressants, and calcium channel blockers, as well as some blood pressure medications, lithium, and antacids that contain aluminum hydroxide.

Clonidine, dopamine agonists, and progesterone are also implicated. So if you have gastroparesis, your symptoms could improve if you move off those medications under the care of your doctor. Nicotine is also associated with impaired gastric emptying, so you might want to quit smoking.

Especially in people with diabetes, it's critical to regain control of blood sugar levels that are out of whack, especially because better control of blood sugar levels can actually improve stomach emptying. Sometimes it can help to take insulin after meals instead of before. Testing more frequently will allow you to take insulin in response to blood glucose levels as they rise, rather than in response to a meal that might just take awhile to hit the bloodstream. Your doctor can advise you about methods to bring your blood sugars down and, hopefully, relieve your gastroparesis.

There are a number of drugs available to treat gastroparesis: Some of them relieve nausea and vomiting; others ease abdominal pain. Others still, called pro-motility drugs, stimulate contractions of the stomach muscles. There's also the rather new possibility of getting a pacemaker for your stomach, which generates electrical pulses that stimulate the wave-like muscle contractions you need to get things moving again.

The latest (and still experimental) treatment is injection of botulinum toxin (Botox) into the pylorus; just like it does to your forehead wrinkles, the Botox temporarily relaxes the powerful pyloric muscle, thereby enlarging the outlet from the stomach to the intestine and allowing the release of more food.

Gastroparesis is not usually life-threatening, but it can really put a dent in your quality of life and make your diabetes much harder to control. There's been a lot of progress made recently in treatments for the condition, so think about taking a trip to your doctor or gastroenterologist. It just might get things moving along in the right direction. www.diabeteshealth.com/read/2007/06/30/5283.html___________________

Gastroparesis
Medical Revising Author: Dennis Lee, MD
Medical Revising Editor: Jay W. Marks, MD

What is gastroparesis?
What are gastroparesis symptoms and signs?
What causes gastroparesis?
How is gastroparesis diagnosed?
How is gastroparesis treated?
What is the prognosis (long-term outcome) for patients with gastroparesis?
What's new in gastroparesis?
Gastroparesis At A Glance
What is gastroparesis?

Gastroparesis means paralysis of the muscles of the stomach. Gastroparesis results in delayed emptying of food from the stomach into the small intestine.

The stomach is a hollow organ composed primarily of muscle that serves as a storage container for food. Food in the stomach is ground into tiny pieces by the constant churning that is generated by the contractions of the stomach’s muscles. Once the food has been adequately ground, it slowly is emptied from the stomach into the intestine in a metered fashion. Only food ground into small particles can be emptied from the stomach in a normal fashion, and smaller particles are digested better in the intestine. Moreover, the metering process allows the emptied food to be well-mixed with the digestive juices of the intestine, pancreas, and liver (bile) and to be absorbed well from the intestine.

When the stomach’s muscles are paralyzed, food is not thoroughly ground and does not empty into the intestine normally. Since the muscular mechanisms whereby ground, solid food and liquid food are emptied from the stomach are different, there may be delayed emptying of solid food (most common), solid and liquid food (less common), or liquid food alone (least common).

What are gastroparesis symptoms and signs?

The primary symptoms of gastroparesis are nausea and vomiting. Other symptoms of gastroparesis include abdominal pain, bloating, early satiety (feeling full quickly when eating), and in severe cases, weight loss due to a reduced intake of food because of the symptoms. Reduced intake of food and restriction of the types of food that are eaten can lead to nutritional deficiencies.

The vomiting of gastroparesis usually occurs after meals; however, with severe gastroparesis, vomiting may occur without eating due simply to the accumulation of secretions in the stomach. The characteristic vomiting happens several hours after a meal when the stomach is maximally distended by the presence of food and secretions stimulated by the meal. Since the grinding action of the stomach is absent, the vomited food often remains in larger pieces and is easily recognized. (Contrast this with the more common type of vomiting in which the food appears as small, uniform, unidentifiable particles.)

Other, less frequent effects of gastroparesis are the promotion of gastroesophageal reflux disease (GERD) and malnutrition.

What causes gastroparesis?

Gastroparesis can be caused either by diseases of the stomach’s muscles or the nerves that control the muscles, though often no specific cause is identified. The most common disease causing gastroparesis is diabetes mellitus which damages the nerves controlling the stomach muscles. Gastroparesis also can also result from damage to the vagus nerve, the nerve that controls the stomach’s muscles, that occurs during surgery on the esophagus and stomach. Scleroderma is an example of a disease in which gastroparesis is due to damage to the stomach’s muscles. Occasionally, gastroparesis is caused by nervous reflexes, for example, when the pancreas is inflamed (pancreatitis). In such cases, neither the nerves nor the muscles are diseased, but messages are sent through nerves from the pancreas to the stomach which prevents the muscles from working normally.

Other causes of gastroparesis include imbalances of minerals in the blood such as potassium, calcium or magnesium, medications (such as narcotic pain-relievers), and thyroid disease.

Gastroparesis can occur as an isolated problem or it can be associated with paralysis of other parts of the intestine, including the esophagus, small intestine, and colon.

How is gastroparesis diagnosed?

The most common method for diagnosing gastroparesis is a nuclear medicine test called a gastric emptying study which measures the emptying of food from the stomach. For this study, a patient eats a meal in which the solid food, liquid food, or both contain a small amount of radioactive material. A scanner (acting like a Geiger counter) is placed over the stomach for several hours to monitor the amount of radioactivity in the stomach. In patients with gastroparesis, the food takes longer than normal (usually more than several hours) to empty into the intestine.

The antro-duodenal motility study is a study that can be considered experimental that is reserved for selected patients. An antro-duodenal motility study measures the pressure that is generated by the contractions of the muscles of the stomach and intestine. This study is conducted by passing a thin tube through the nose, down the esophagus, through the stomach and into the small intestine. With this tube, the strength of the contractions of the muscles of the stomach and small intestine can be measured at rest and following a meal. In most patients with gastroparesis, food (which normally causes the stomach to contract vigorously) causes either infrequent contractions (if the nerves are diseased) or only very weak contractions (if the muscle is diseased). An electrogastrogram, another experimental study that sometimes is done in patients with suspected gastroparesis, is similar to an electrocardiogram (EKG) of the heart. The electrogastrogram is a recording of the electrical signals that travel through the stomach muscles and control the muscles' contractions. An electrogastrogram is performed by taping several electrodes onto a patient's abdomen over the stomach area in the same manner as electrodes are placed on the chest for an EKG. The electrical signals are recorded at rest and after a meal. In normal individuals, there is a regular electrical rhythm just as in the heart, and the power (voltage) of the electrical current increases after the meal. In most patients with gastroparesis, the rhythm is not normal or there is no increase in electrical power after the meal. Although the gastric emptying study is the primary test for diagnosing gastroparesis, there are patients with gastroparesis who have a normal gastric emptying study but an abnormal electrogastrogram. Therefore, the electrogastrogram is useful clinically primarily when the suspicion for gastroparesis is high but the gastric emptying study is normal or borderline abnormal.

A physical obstruction to the emptying of the stomach, for example, a tumor that compresses the outlet from the stomach or scarring from an ulcer, may cause symptoms that are similar to gastroparesis. Therefore, an upper gastrointestinal (GI) endoscopy test usually is performed to exclude the possibility of an obstruction as the cause of a patient's symptoms. (Upper GI endoscopy involves the swallowing of a tube with a camera on the end and can be used to visually examine the stomach and duodenum and take biopsies.)

Upper GI endoscopy also may be useful for diagnosing one of the complications of gastroparesis, a bezoar. Because of the poor emptying of the stomach, hard to digest components of the diet, usually from vegetables, are retained and accumulate in the stomach. A ball of undigested, plant-derived material can accumulate in the stomach and give rise to symptoms of fullness or can further obstruct the emptying of food from the stomach. Removing the bezoar may improve symptoms and emptying.

A computerized tomographic (CT) scan of the abdomen and upper gastrointestinal x-ray series may also be necessary to exclude cancer of the pancreas or other conditions that can obstruct the emptying of the stomach.

How is gastroparesis treated?

Treatment of gastroparesis includes diet, medication, and devices or procedures that facilitate emptying of the stomach. The goals of treatment include:

To provide a diet containing foods that are more easily emptied from the stomach.
Controlling underlying conditions that may be aggravating gastroparesis.
Relieve symptoms of nausea, vomiting and abdominal pain.
Stimulate muscle activity in the stomach so that food is properly ground and emptied from the stomach
Maintaining adequate nutrition.
Diet

Emptying from the stomach is faster when there is less food to empty, so smaller, more frequent portions of food are recommended. Soft foods (or preferably liquid) that do not require grinding also are emptied more easily. Moreover, in gastroparesis the emptying of liquids often is less severely affected than the emptying of solids. Fat causes the release of hormones that slow down the emptying of the stomach. Therefore, foods low in fat empty faster from the stomach. In patients with severe gastroparesis, sometimes only liquid meals are tolerated.

Controlling underlying conditions

High levels of glucose (sugar) in blood tends to slow gastric emptying. Therefore it is important to lower blood glucose levels in patients with diabetes to near normal levels with diets and medications. Individuals with a deficiency of thyroid hormone (hypothyroidism) should be treated with thyroid hormone. If bezoars are present, they should be removed (usually endoscopically).

Relieving nausea, vomiting, and abdominal pain

Drugs used to relieve nausea and vomiting in gastroparesis include promotility drugs (see discussion that follows) such as metoclopramide (Reglan) and domperidone, anti-nausea medications such as prochlorperazine (Compazine) and promethazine (Phenergan), serotonin antagonists such as ondansetron (Zofran), anticholinergic drugs such as a scopolamine patch (commonly used for treating motion sickness), drugs used for treating nausea in cancer chemotherapy patients such as aprepitant (Emend), and medical marijuana Marinol.

Drugs used to relieve abdominal pain in gastroparesis include non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Motrin) and naproxen (Aleve), low dose tricyclic antidepressants such as amitriptyline (Elavil), drugs that block nerves that sense pain such as gabapentin (Neurontin), and narcotics such as tramadol (Ultram) and Fentanyl. Narcotic pain relievers as a group tend to cause constipation and slow emptying of the stomach, and, therefore, should be avoided or used with caution among patients with gastroparesis.

Stimulating muscle activity

Oral Drugs. There are four oral drugs that are used to stimulate contractions of the stomach’s muscles, referred to as pro-motility drugs. These drugs are cisapride (Propulsid), domperidone, metoclopramide (Reglan), and erythromycin. Cisapride is an effective drug for treating gastroparesis; however, it was removed from the market because it can cause serious and life-threatening irregular heart rhythms. Despite this fact, it can be obtained for use through the pharmaceutical company that manufactures it (Janssen Pharmaceuticals) under a strictly monitored protocol but only for patients with severe gastroparesis unresponsive to all other measures. Domperidone has not been released for use in the US; however, it can be obtained if approval is obtained for its use from the US Food and Drug Administration. The fourth drug, erythromycin (E-Mycin, Ilosone, etc.), is a commonly-used antibiotic. At doses lower than those used to treat infections, erythromycin stimulates contractions of the muscles of the stomach and small intestine and is useful for treating gastroparesis.

It has been demonstrated that tegaserod (Zelnorm), an oral drug used for treating constipation in irritable bowel syndrome (IBS), increases emptying from the stomach just as it does from the colon. However, in March of 2007, the FDA asked Novartis to suspend sales of tegaserod (Zelnorm) in the United States because a retrospective analysis of data by Novartis from more than 18,000 patients showed a slight difference in the incidence of cardiovascular events (heart attacks, strokes and angina) among patients on Zelnorm compared to placebo. The data showed that cardiovascular events occurred in 13 out of 11,614 patients treated with Zelnorm (.11%), compared to one cardiovascular event in 7,031 (.01%) placebo-treated patients. However, it is unclear whether Zelnorm actually causes heart attacks and strokes. Doctors and scientists will be scrutinizing the data to determine the long term safety of Zelnorm.

Further studies will be necessary to determine just how effective tegaserod is and how it compares to the other medications that are available for treating gastroparesis before its use can be recommended.

There are two important guidelines in prescribing oral drugs for gastroparesis. First, the drugs must be given at the right times, and second, the drugs must reach the small intestine so that it can be absorbed into the body. Since the goal of treatment is to stimulate muscular contractions during and immediately after a meal, drugs that stimulate contractions should be given before meals.

Most drugs must be emptied from the stomach so that they can be absorbed in the small intestine. The majority of patients with gastroparesis have delayed emptying of solid food, and pills and capsules, like solid food, do not empty well from the stomach. As mentioned previously, many patients with gastroparesis have less of a problem emptying liquids as compared with solid food. Therefore, liquid medications usually are more effective than pills or capsules.

Intravenous drugs. Occasionally, patients have such poor emptying of both liquid and solid food from the stomach that only drugs given intravenously are effective. In such patients, intravenous metoclopramide or erythromycin can be used. A third option is octreotide (Sandostatin), a hormone-like drug that can be injected beneath the skin. Like erythromycin, octreotide stimulates short bursts of strong contractions of the muscles in the stomach and small intestine. Due to its greater expense and the need for injection, octreotide is used only when other medications fail.

Electrical pacing. Electrical pacing of the stomach is a new method for treating severe gastroparesis. Electrical pacing of the stomach is analogous to cardiac pacing for the treatment of an abnormally slow heartbeat and involves the placement of a pacemaker. The pacemaker usually is placed laparoscopically and does not require a large abdominal incision for entering the abdomen. During placement, wire electrodes are attached to the muscle of the stomach. The wires are brought out through the abdominal wall just beneath the skin. The wires are attached to a small, battery-operated pacemaker that is buried in a surgically-created pouch just under the skin. The skin is then sutured so that the pacemaker and wires are beneath the skin. The pacemaker generates electrical impulses that are transmitted by the wires to the muscles of the stomach, and the muscles contract in response to the impulses. Electrical pacing is effective in many patients with severe gastroparesis, but the numbers of patients who have been treated is small. Since electrical pacing of the stomach is relatively new, the long-term effectiveness and safety have not been determined clearly.

Surgery. Surgery occasionally is used to treat gastroparesis. The goal of surgery is to create a larger opening between the stomach and the intestine in order to aid the process of emptying the stomach's contents. Alternatively, the entire stomach may be removed. These procedures should be considered only when all other measures have failed because of the potential complications from the surgery. Surgery should be done only by surgeons in consultation with gastroenterologists who are knowledgeable and experienced in caring for patients with gastrointestinal motility disorders (disorders of the nerves or muscles of the gastrointestinal tract that affect digestion and transport of food).

Maintaining nutrition

Patients with mild gastroparesis usually can be successfully managed with pain relievers and pro-motility medications, but patients with severe gastroparesis often require repeated hospitalizations to correct dehydration, malnutrition and to control symptoms.

Treatment options for dehydration and malnutrition include:

Intravenous fluids to correct dehydration and replenish electrolytes if nutrition is adequate but symptoms occasionally interrupt the intake of even liquid food.
Enteral nutrition which provides liquid food directly into the small intestine, bypassing the paralyzed stomach.
Intravenous total parenteral nutrition (TPN) to provide calories and nutrients (TPN is a fluid containing glucose, amino acids, lipids, minerals, and vitamins—everything that is needed for adequate nutrition—intravenously. The fluid usually is delivered into a large vein via a catheter in the arm or upper chest.)
Doctors generally prefer enteral nutrition over TPN because long-term use of TPN is associated with infections of the catheter and liver damage. Infection can spread through the blood to the rest of the body, a serious condition called sepsis. Catheter-related sepsis often requires treatment with intravenous antibiotics and removal of the infected catheter or replacement with a new catheter. TPN also can damage the liver, most commonly causing abnormal liver tests in the blood. TPN-induced liver damage usually is mild and reversible (the liver test abnormalities return to normal after cessation of TPN), but, rarely, irreversible liver failure can occur. Such liver failure may require liver transplantation.

Enteral nutrition is safe and effective. The two common means of delivering enteral nutrition are via naso-jejunal tubes or jejunostomy tubes. The jejunum is the part of the small intestine just past the duodenum, the first part of the small intestine just beyond the stomach. Both naso-jejunal tubes and jejunostomy tubes are designed to bypass the stomach and deliver nutrients into the jejunum where they can be absorbed.

A naso-jejunal tube is a long, thin catheter inserted (usually by a radiologist or a gastroenterologist) via the nostril into the stomach. The tip of the naso-jejunal tube is then advanced past the stomach into the small intestine. Often this must be done during upper GI endoscopy. Liquid nutrients then can be delivered via the naso-jejunal tube into the small intestine. Naso-jejunal tubes generally are safe, but there are cosmetic disadvantages and discomfort of having a tube in the nose. The problems that occur with naso-jejunal tubes are primarily accidental or intentional removal by the patient, blockage of the tube by solidified nutritional solutions, and aspiration (backup of stomach contents into the lungs that can lead to pneumonia).

A jejunostomy is a catheter placed directly into the jejunum. It can be done during standard abdominal surgery, using minimally invasive techniques (laparoscopy), or by a specially-trained radiologist. With a jejunostomy, the catheter passes through the skin on the abdominal wall and directly into the jejunum. Before a jejunostomy is placed, a trial of naso-jejunal nutrition often is given to be certain that the small bowel is not involved with the same motility problem as the stomach and that nutritional liquids infused into the small intestine will be tolerated.

What is the prognosis (long-term outcome) for patients with gastroparesis?

If gastroparesis is caused by a reversible problem, for example pancreatitis, the condition will subside when the underlying problem resolves. In some diabetics, better control of their blood sugar will improve emptying of the stomach. If there is no reversible cause, gastroparesis rarely resolves. In fact, it may become worse with time. Gastroparesis is particularly difficult to treat when there are accompanying motility disorders of the muscles of the small intestine.

What is new in gastroparesis?

The newest experimental treatment for gastroparesis is injection of botulinum toxin into the pylorus. The pylorus is the narrow channel through which food passes from the stomach to the duodenum. The pylorus, like the stomach, is a muscular organ. The pylorus is closed most of the time due to continuous contraction of the pyloric muscle. Intermittently it opens and allows secretions from the stomach to enter the small intestine. After meals, the pylorus is very important for metering the emptying of the stomach. In gastroparesis, although the muscles of the stomach are weak all of the time, the muscle of the pylorus remains strong and contracted and the pylorus relatively closed. It was hypothesized that if the strength of the pyloric muscle was reduced, food might empty from the stomach more readily. Although a surgical procedure, termed pyloroplasty, to enlarge the pylorus has been used in the past to treat problems with emptying of the stomach, it is major surgery and has had mixed results with respect to its efficacy. More recently, relaxation of the pyloric muscles has been produced by injecting botulinum toxin (Botox) into the pylorus. Although results have been good, the procedure has not been studied enough to recommend its use unless it is part of a research protocol.

Gastroparesis At A Glance
Gastroparesis is a disease of the muscles of the stomach or the nerves controlling the muscles that causes the muscles to stop working.
Gastroparesis results in inadequate grinding of food by the stomach and poor emptying of food from the stomach into the intestine.
The primary symptoms of gastroparesis are nausea and vomiting.
Gastroparesis is best diagnosed by a test called a gastric emptying study.
Gastroparesis usually is treated with nutritional support, drugs for treating nausea and vomiting, drugs that stimulate the muscle to contract, and, less often, electrical pacing and surgery. http://www.medicinenet.com/gastroparesis/page5.htm

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