Thursday, August 30, 2007

Dr Sutherland



Director of the Diabetes Institute for Immunology and Transplantation
Head of the Transplant Division in the Department of Surgery
Holder of the Golf Classic "fore" Diabetes Research Chair
Professor of Surgery at the University of Minnesota

As a young resident, Dr. David E.R. Sutherland witnessed the makings of a miracle in 1966 at the hands of Drs. Richard Lillehei and William Kelley, who performed the world's first kidney-pancreas transplant in a patient with diabetes. Convinced that this surgery could be refined and offer a better quality of life to people with diabetes, Dr. Sutherland embarked on a career devoted to availing pancreas transplants for those wanting this procedure.

Since 1978, he has routinely offered whole-organ pancreas transplantation, and has trained 90% of surgeons performing this procedure worldwide. His teachings has affected countless others in the field of immunology and transplantation, yielding several other unique pancreas surgeries not performed routinely at other institutions.

Dr. Sutherland performed the world's first transplant of insulin-producing islet cells from a deceased human donor to a living person in 1974. He also has developed specialized surgeries to prevent the onset of diabetes upon the removal of a pancreas in the case of chronic pancreatitis.

Dr. Sutherland performed the world's first living-donor (segmental) pancreas transplant in 1979. He and his team continue to perform more of these complex surgeries than any other program worldwide, offering the potential of a higher quality of life for patients facing severe health issues from diabetes and pancreatitis.

Dr. Sutherland is a surgeon, researcher, pioneer, administrator, leader, mentor, professor, and respected colleague to thousands worldwide.

For nearly 40 years, he has diligently worked to achieve a higher quality of life for people with diabetes, freeing many from the major secondary health issues caused by diabetes, such as blindness, kidney failure, nerve damage, and cardiovascular disease.

Thanks to Dr. Sutherland's dedication and perseverance, the University of Minnesota has achieved worldwide prominence as a center of hope and excellence for people with diabetes. The University of Minnesota is the home of the world's oldest, largest pancreas transplant program. He has earned international recognition for the successful transplantation of insulin-producing tissue called islets, normalizing blood sugar levels in people devastated by diabetes.

Dr. Sutherland, M.D., Ph.D., is a Professor of Surgery at the University of Minnesota. In addition, he is the Head of the Transplant Division and the Director of the Diabetes Institute for Immunology and Transplantation. Dr. Sutherland holds the Gold Classic "fore" Diabetes Research Chair. He is also on the executive committee of the Collaborative Islet Transplant Registry (CITR), which is funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Dr. Sutherland has served as president of the International Transplantation Society, the American Society of Transplant Surgeons, the Cell Transplant Society, and the International Pancreas and Islet Transplant Association.

If you would like to make a contribution to help support Dr. Sutherland's diabetes research, feel free to use our on-line gift form. Please be sure to specify the DIABETES INSTITUTE in Step 2 of this form. If you would like to discuss your charitable goals, please contact Angela Lillie at 612-626-2101.

Sunday, August 26, 2007

Movement of the Pancreas Associated with Change of Posture

Posted by cj on August 25, 2007 at 22:03:50:


MULTIMEDIA ARTICLE - Clinical Imaging


Article in PDF format - JOP Home page

JOP. J Pancreas (Online) 2007; 8(4):458-459.


Movement of the Pancreas Associated with Change of Posture


Deepak Kumar Bhasin, Surinder Singh Rana, Birinder Nagi, Saroj Kant Sinha, Kartar Singh


Department of Gastroenterology, Post Graduate Institute of Medical Education and Research (PGIMER), Sector 12. Chandigarh, India

Because of its deep retroperitoneal location, the pancreas and swellings arising from it have been considered to be immobile during respiration as well as during change of posture [1, 2]. However, we, as well as other authors worldwide, have demonstrated that the traditional belief of the immobility of the pancreas during respiration is not true and, indeed, the pancreas moves during respiration [3, 4, 5, 6]. The phenomenon of the movement of the pancreas when changing posture has also been reported earlier [7]. We were intrigued with the marked mobility of the pancreas which was encountered during change of posture in a 25-year-old female patient with idiopathic chronic calcific pancreatitis.

This 25-year-old female presented to us with acute abdominal pain of 24-hour duration. As a part of the diagnostic evaluation, abdominal skiagrams were performed both in the erect and the supine position which showed dense pancreatic calcification. This pancreatic calcification demonstrated marked movement during change of posture from the supine to the erect position. Once the patient recovered from an acute episode of abdominal pain, the skiagrams of the abdomen were repeated in both erect and supine positions, with the patient holding her breath in mid-expiration, to confirm the movement of the pancreas during change of posture. The skiagrams were performed after repeated rehearsals of breath holding in the same phase of respiration (mid-expiration) to negate the effect of respiration on the movement of the pancreas. The abdominal skiagram in the supine position showed dense calcification throughout the pancreas (Image 1). The abdominal skiagram in the erect position (Image 2) showed a marked downward as well as a medial movement of the pancreas during change of posture from the supine to the erect position.

Image 1.








Image 2.






This phenomenon of movement of the pancreas during respiration as well as during change of posture dispels the traditional belief that the pancreas, being a retroperitoneal organ, is fixed and does not move either during respiration or during change of posture. This may have important implications for imaging, and guided diagnostic and therapeutic minimally invasive interventions such as focusing on pancreatic duct stones during treatment with extracorporeal shockwave lithotripsy (ESWL) as well as accurate placement of the needle during percutaneous fine needle aspiration biopsy and other minimally invasive interventions.

References

Williams PL, Warwick R, Dyson M, Bannister LH, eds. Gray's Anatomy. 37th edition. Edinburgh, UK: Longman Group, 1989; 1380-4. [More details]

Swain P. The gastrointestinal tract and abdomen. In: Swash M, ed. Hutchison's Clinical Method's. 20th edition, London: WB Saunders, 1995:75-116. [More details]

Bhasin DK, Rana SS, Jahagirdar S, Nagi B. Does the pancreas move with respiration? J Gastroenterol Hepatol 2006; 21:1424-7. [More details]

Suramo I, Paivansalo M, Myllyla V. Cranio-caudal movements of the liver, pancreas and kidneys in respiration. Acta Radiol Diagn (Stockh) 1984; 25:129-31. [More details]

Bryan PJ, Custar S, Haaga JR, Balsara V. Respiratory movement of the pancreas: an ultrasonic study. J Ultrasound Med 1984; 3:317-20. [More details]

Bhasin DK, Rana SS, Chandail VS. The pancreas and respiration: oblivious to the obvious! JOP. J Pancreas (Online) 2006; 7:578-83. [More details]

Morgan RA, Dubbins PA. Pancreatic and renal mobility. Clin Radiol 1992; 45:88-91. [More details]

Article in PDF format


--------------------------------------------------------------------------------

Received February 24th, 2007 - Accepted March 29th, 2007

Keywords Cholangiopancreatography, Endoscopic Retrograde; Lithotripsy; Pancreatic Pseudocyst; Pancreatitis; Tomography, X-Ray Computed

Conflict of interest The authors have no potential conflicts of interest

Correspondence
Deepak Kumar Bhasin
1041, Sector 24-B,
Chandigarh
160 023, India
Phone: +91-172.272.5056; +91-172.271.5870
Fax: +91-172.274.4401
E-mail: deepakkbhasin@gmail.com; dkbhasind@hotmail.com



JOP Home page


http://www.joplink.net/

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.
_________________________________________________________
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

Lab results, help?

Posted by laurie on August 17, 2007 at 23:30:20:
In Reply to: Lab results, help? :) posted by Tina on August 16, 2007 at 19:14:25:


As far as your lab values: I will start out with a qualifier - I do not know what is considered "normal" for someone who has gone through the surgery you have so take what I write with that thought is mind. But.....

in a "normal" person (ie not post-op from pancreas surgery with the ICT to the liver)....these LFTs are not considered significantly raised. The rule of thumb for normal people are that values that are 1.5 to 2 time above the high cutoff point are considered to be significant. Those that are >2x but less than about 5x are looked at as somewhat concerning. Those that are 5x to about 10x are followed-up with a little more urgency; those that are >10x the high end of normal are considered alarming and can be "critical" in the right context.

Slight LFTs elevations like yours can be normal due to personal differences like body weight, diet, medication etc. In your case, I am just guessing here but I would suspect that they are slightly up due to your recent surgery - you are sill recuperating from the anesthesia and the insult to the liver from the islet cell transplant. You most likely have some inflammation that needs to heal yet. Or some of the meds you are taking (any tylenol?) could cause this.

As far as your BUN - again, I could be wrong but it is a high BUN that is cause for concern. A low BUN is nothing to be worried about and may even mean your kidneys are super efficient by clearing your urea better than "normal"... but again, I do not know if in light of your surgery if it has other significance that may not be seen in "normal" people.

Speaking from experience with abdominal surgery that involves the pancreas (but I did not have the exact surgery you had so again, interpret this cautiously)...I can say that pain-wise it can take some time to stabilize. That there will be ups and downs for quite a while. I honestly feel it took about a year, maybe more, for me to feel even half-way recovered from my surgery. It may be too soon to be thinking about going back to have the rest of your pancreas removed. Give it some time yet and if you have to use your pain meds again don't feel like you have taken a step back. By becoming comfortable you will speed up the healing process and make it that more likely to have a successful outcome from this one surgery alone. Of course all of my "advice" is nonsense if your symptoms get worse....

laurie

Decompression surgery for pain

Posted by cj on August 19, 2007 at 13:34:06:
In Reply to: decompression surgery for pain posted by Lori on August 19, 2007 at 12:47:55:


Treatment
Patients with disabling abdominal pain, evidence of chronic pancreatitis, and pancreatic ductal dilatation are best managed by pseudocyst decompression or ductal decompression (Puestow panceraticojejunostomy procedure), while patients without ductal dilatation are best treated with resection. Biliary-enteric decompression may also be required in patients with chronic pancreatitis and bile duct obstruction. Although preservation of pancreatic tissue is desired to maintain both exocrine and endocrine function, partial pancreatic resection (such as distal pancreatectomy ,pancreaticoduodenectomy, or duodenal preserving pancreatic head resection/decompression [i.e. Beger or Frey procedures]) is at times the preferred treatment. While alternative procedures such as endoscopic sphincterotomy, short-term stent placement in the major pancreatic duct or pancreatic pseudocyst, may provide short-term relief of symptoms; long-term results are as yet unknown.

http://www.ssat.com/cgi-bin/chrpanc6.cgi

AS far as barring you from further surgery (ie.TP/ICT) you could still have it done but with less islet cells to harvest. ALL Surgeries to pancreas reduce outcome of TP/ICT surgery. ALSO it is been told to us that the surgery for a Whipple/puestow is more rigorous on the body than just having the tp done. I would guess that being that the pancreas is so sensitive (just ercps can cause horrific attacks) that cutting on it would totally TICK the pancreas to the Nth degree on top of trying to heal from the surgery itself

Minimal Change Chronic Pancreatitis

Posted by Robin H. (CA) on August 23, 2007 at 12:46:37:


DEAR LISTMATES: Here is a written response by Dr. Sutherland himself and an article by Dr. Sutherland's research group about "minimal change CP". It clearly states that you can have "microscopic CP" that causes horrible pain, yet does not yield positive diagnostic results on an EUS. I am posting this in response to recent posts that have suggested that THERE IS A PREVAILING MOVEMENT TO PUSH THE TP/ICT and that it is better to wait for emerging diagnostic criteria on an EUS, which for those patients like me, who had "Minimal Change CP", would have resulted in a less than beneficial islet cell yield.
I enclose an excerpt (below) from an email from Dr. Sutherland himself regarding this matter.
***********************************************************
There are articles on minimal change CP that I will send you the references. We also have an abstract showing that the traditional view that an EUS has to show 5 of 9 criteria for CP to be diagnosed is not correct, even one criteria has been associated with documented CP under the microscope.

Many patients have had acute relapsing pancreatitis for years, pain free between episodes, and now began go have constant pain and go on daily narcotics. At 6 months of narcotics and pain getting worse, what would one propose even if imaging shows only minimal changes.

The fact is that 95% of our patients say they are better off, whether done early or late, and all done late wish they had done it earlier. Ann Marie can give you names of patients who might be interested n chiming in in.

Attached is an abstract summarizing outcomes with TP/IAT at Minnesota, along with a review article we have written on the topic, and you should feel free to share these on the web.

Pancreas Club, Inc. 41st Annual MeetingSunday, May 20, 2007Washington, DC

ABSTRACT FORM

Abstract Revised: July 31, 2007
Title of abstract: Pancreatectomy and autologous islet transplantation: a study of long-term outcomes
Authors: Annelisa M. Carlson MD, Juan J. Blondet MD, Angelika Gruessner PhD, Melena Bellin MD, Greg Beilman MD, David E.R. Sutherland, MD, PhD
Institution: University of Minnesota, Departments of Surgery and Pediatrics
Presentation of abstract, if accepted: (please choose one)
0 Oral presentation 0 Poster presentation x Oral or Poster presentation
Corresponding Author: Annelisa M. Carlson, MD
Presenting Author: David E.R. Sutherland, MD, PhD
Mailing address: Department of SurgeryUniversity of Minnesota Medical SchoolMMC 280, 420 Delaware Street S.E.Minneapolis, MN 55455
TEL: 612-625-7600 FAX: 612-624-7168 EMAIL: dsuther@umn.edu

Program Chairman: William H. Nealon, MDUTMB Department of Surgery6.112 John Sealy HospitalGalveston, TX 77555-0544Tel: (409) 772-6582 Fax: (409) 747-2253E-mail: wnealon@utmb.edu
For more information, please visit our website at www.pancreasclub.com.
ABSTRACT(Not to exceed 1 full page. May include graphs, charts, and/or images.)


Pancreatectomy and autologous islet transplantation: a study of long-term outcomes Annelisa M. Carlson, Juan J. Blondet, Angelika Gruessner, Melena D. Bellin, Greg Beilman, David E.R. Sutherland Departments of Surgery and Pediatrics, University of Minnesota Minneapolis,

MN 55455
INTRODUCTION
Pancreatectomy with autologous islet transplantation (TP/IAT) is performed to alleviate pain and improve quality of life of patients with severe chronic pancreatitis who have failed prior medical and oftentimes surgical therapies; the islet autograft is performed with a goal of preventing post-surgical diabetes.

The aim of this study was to examine long-term outcomes with regard to pain, quality of life, and graft function.

METHODS
We performed 188 pancreatectomies with islet autografts (25 children, 5-18 yrs) during the period from Feb,1977-Sep,2006. Medical records were reviewed, and patients were contacted to complete a telephone survey. Patients were classified as having full graft function if they reported complete insulin-independence;
partial graft function if on a once-daily long-acting insulin;
and graft failure if on a full diabetic regimen.

Islet function rates were computed using Kaplan-Meier estimates.RESULTSIn the entire series, patient survival rates after TP/IAT were 98% at 1 yr, 92% at 3 yrs, 87% at 5 yrs and 73% at 10 years. Eighty-three adult patients were able to be reached for the telephone survey (71% female, 29% male; mean age 37 +/- 10 years), at a median of 42 months post-TP/IAT (range 2-330 months). Etiologies of pancreatitis included idiopathic (60%), alcohol (17%), pancreas divisum (12%), biliary (7%), and hereditary (5%). Total pancreatectomy was performed in 68%, partial or distal in 11%, completion in 17%, and near-total in 4%.
One-hundred percent of adult patients stated they had pancreatitis pain prior to undergoing TP/IAT;
93% stated they were on daily narcotics prior to TP/IAT.
Ninety-four percent reported an improvement in pain following the procedure, and 49% of patients have been able to discontinue daily narcotic pain medications.
Ninety-six percent of patients would recommend the procedure.
Eighty-five percent of adult patients stated their quality of life has significantly improved compared to the time before their TP/IAT, while 8% state their quality of life is the same, and 5% (n=4) stated it is worse.

In the overall series, full and partial graft function was seen in 74% of adult patients at 1 year and 70% at 5 years; full graft function alone was seen in 55% of patients at 1 year, 40% at 5 years and 34% at 10 years.
Patients who had undergone a previous pancreatic resection had a significantly lower islet yield than those who had not (2712 IEQ/kg versus 4077 IEQ/kg, p=0.0.03). When adjusted according to islet mass (IE) transplanted, there were virtually no adult cases of insulin-independence when <2500 IE/kg were transplanted, while it was 47% with 2500-5000 IE/kg (n=27) and 75% with >5000 IE/kg (n=21).
IAT function for more than 16 hears has been documented in at least 2 adult cases, showing the potential for durable engrafment.Of the pediatric patients, all had been on narcotics preoperatively, while only 39% were on at follow-up. 94% reported improvement in pain, and 67% were entirely pain free. At 1 yr after TP/IAT, 78% had full or partial islet function and 56% were insulin-independent. The mean islet yield (IEQ/kg) was 7467 for those with full, 4066 with partial and 2890 with poor/no graft function, but there was considerable overlap and some low yields functioned well. The likelihood of insulin-independence was 67% in those without and only 33% in those with previous direct surgery on the pancreas.

CONCLUSIONS
TP/IAT can ameliorate pain and improving quality of life long term in most patients with CP in whom other interventions have failed. The islet autograft prevents or minimizes post-surgical diabetes in about 2/3 of patients and insulin-independence is sustained long-term in about 1/3. Narcotic induced hyperalgesia from prolonged use prior to TP/IAT prevents a substantial proportion of patients from withdrawing even when the pancreatic pain is relieved. Islet yield and function and ease of narcotic withdrawal may be improved if patients are referred for TP/IAT earlier in the course of their disease. Patients with chronic pancreatitis who have persistent pain after standard interventions should be considered for TP/IAT, and ideally should not be on narcotic analgesics for > 6 months without being referred..

CONTROL ID: 317038
CATEGORY: Endoscopic Ultrasound
PRESENTATION TYPE: ASGE Oral or Poster
PRESENTER: Kapil Gupta
PRESENTER (E-MAIL ONLY): gupta078@umn.edu
Abstract
TITLE: EUS early chronic pancreatitis: Comparison with histopathology in patients undergoing total pancreatectomy with autologous islet cell transplantation

AUTHORS (LAST NAME, FIRST NAME): Gupta, Kapil1, 2; Carlson, Annelisa3; Kobayashi, Takashi3; Manivel, Carlos4; Lai, Rebecca1, 2; Mallery, Shawn1, 2; Sutherland, David E.3; Freeman, Martin L.1, 2
INSTITUTIONS (ALL): 1. Gastroenterology, University of Minnesota, Minneapolis, MN, USA. 2. Gastroenterology, Hennepin County Medical Center, Minneapolis, MN, USA. 3. Surgery, University of Minnesota, Minneapolis, MN, USA. 4. Pathology, University of Minnesota, Minneapolis, MN, USA.

ABSTRACT BODY:
Background: The diagnosis of minimal change chronic pancreatitis (CP) is challenging. The role of endoscopic ultrasonography (EUS) is controversial. At least 3-5 out of 9 possible EUS criteria are generally required to suggest this diagnosis. No previous series comparing EUS with histopathology has included significant numbers of patients with minimal change or non-calcific CP.Aim: To compare EUS imaging to histology in patients with clinically suspected CP undergoing total pancreatectomy with autologous islet cell transplantation (TP/ AIT).Methods: All patients who underwent EUS prior to TP/ AIT for intractable abdominal pain and suspected minimal change chronic pancreatitis were reviewed. EUS was performed by two expert endosonographers. Pancreatic histology was analyzed by a gastrointestinal pathologist with expertise in pancreatic pathology. Results: Of the 15 patients studied, 14 (93%) were women. Ages ranged from 14 to 44 years (mean 33). Histologic exam revealed fibrosis in 14/15 (93%) [7 mild, 5 moderate, 2 severe]; parenchymal atrophy in 9/15 (60%) [4 mild, 3 moderate, 2 severe]; inflammation in 10/15 (67%) [7 mild, 1 moderate, 2 severe]. All 15 patients had at least one of the above histopathologic abnormalities, and all patients responded clinically with improvement or resolution of pain after TP/AIT. Three or more criteria for CP on EUS were present in 10 (67 %); all 10 of these patients had fibrosis [6 mild, 4 moderate to severe]; 7 had atrophy (3 mild, 4 moderate to severe); inflammation in 5 (4 mild, 1 severe). Less than 3 criteria were present in 5 patients; fibrosis was present in 4, all of moderate severity; atrophy in 2, and inflammation in 5. In the one patient with no EUS criteria, the only histopathologic finding was mild acute inflammation. There was no apparent or statistically significant association between mean number of EUS criteria and severity of histological changes (Table 1). Conclusion: In our pilot study there is a subset of patients who have clinical and histological evidence of chronic pancreatitis with minimal (<3) EUS criteria. The severity of histological changes did not correlate with number of EUS criteria. These preliminary findings bring into question the sensitivity and clinical utility of EUS for the diagnosis of minimal change or non-calcific CP. A prospective study evaluating the role of EUS in diagnosis of CP, and its correlation with histopathology is ongoing.
Table 1: Mean number of EUS criteria None or Mild/Minimal changes Moderate to severe changes
Fibrosis 3.6 (0-6) 3.3 (2-5)
Atrophy 3.5 (0-6) 3.4 (2-5)
Inflammation 3.6 (0-6) 3 (2-4)

(No Image Selected)
ASGE Questions
ASGE Minority or Gender Study: No
NASPHGAN Pediatric Endoscopy Award: No
Disclosures
ASGE - Disclosure Form:
Kapil Gupta: No financial interests exist.
Annelisa Carlson: No financial interests exist.
Takashi Kobayashi: No financial interests exist.
Carlos Manivel: No financial interests exist.
Rebecca Lai: No financial interests exist.
Shawn Mallery: No financial interests exist.
David Sutherland: No financial interests exist.
Martin Freeman: No financial interests exist.

Thursday, August 16, 2007

Genetic Testing

Posted by cj on August 15, 2007 at 23:15:23:
In Reply to: Genetic Testing posted by Lori on August 15, 2007 at 09:15:56:


Jerry had his genetic testing done thru the University of Pittsburg. EVEN though he did not test positive for any of the genes, being that he has several family members with the same problem, they do not exclude hereditary links. The lady explained to me that they had HUNDREDS of families with multiple pancreatic patients and there is a definate link that doesnt fit the ones they know of but they know somehow they are linked.

http://www.pancreas.org/

The issues surrounding genetic testing of patients with suspected hereditary pancreatitis or other gene mutations is complex (see discussion by Etamad and Whitcomb). Several major research trials are underway and information will be forwarded to physicians by request by emailing Beth Elinoff.

Complete screening of the CFTR gene is available at a fraction of the cost of direct sequencing is now available at Ambry Genetics.

Ambry Genetics has now developed a complete pancreatitis panel of genetic testing that covers ALL regions of trypsinogen (PRSS1), pancreatic secretor trypsin inhibitor (SPINK1) and the cystic fibrosis transmembrane conductance regulator (CFTR). Contact information is

Ambry Genetics
100 Columbia, suite 200
Aliso Viejo, California 92656
Main # 949-900-5500
Fax # 949-900-5501

CLIA#: 05D0981414
California Lab ID#: CLF 11694

Part 2

http://www.pancreas.org/patients/patients_genetictesting.html

Genetic Testing for Hereditary Pancreatitis

Careful consideration should be made when considering genetic testing for any condition. Some of the considerations are discussed in the Frequently Asked Questions page or in a Consensus Statement from 2001. Not that recent progress has been made in the diagnosis of all forms of recurrent acute and chronic pancreatitis and that we now recommend CFTR and SPINK1 testing as well as trypsinogen testing. Note: genetic testing for trypsinogen mutations has been exclusively licensed to Ambyr Genetics.
Genetic testing for HP

Genetic testing for HP is currently available only on a commercial basis. Commercial testing is conducted through a licensed laboratory (Ambry Genetics) for a specified fee that may be covered by your insurance plan. A small blood sample is drawn at your doctor's office or hospital laboratory and sent to the commercial laboratory for testing. Results are then provided to your referring physician or counselor. Check with your insurance carrier to determine whether genetic testing is covered by your health plan.
Testing can only be done in a laboratory licensed to perform this test.

If testing is being done at other institutions within the United States, please call the 888- PITT DNA number to be sure that the site is approved. Genetic testing for any condition is a complex process. Genetic counselors should be available in your local area to help identify the potential risks, benefits, and limitations of genetic testing for HP. Referrals to local genetic counselors can be obtained from your primary care physician. To find a genetic counselor near you, ask your physician or call us for assistance at 888-PITT-DNA.

Monday, August 13, 2007

In Reply to: 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

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.

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
GastroparesisMedical 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 GlanceGastroparesis 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

Tuesday, August 07, 2007

What is the treatment for dehydration? And what are ways of preventing dehydration?

Posted by RobertMoore65 on August 06, 2007

Just some info I received from one of my gastro docs. I was having a little trouble with the bathroom trotts. Knowing this has led to dehydration and a pancreas flair in the past, I wanted to avoid it if at all possible. I was trying to use OTC Immodium without much luck. So I started with the Poweraid to try and replace the fluid and electrolytes. The doctor explained that sports drinks are not the best way to approach re hydration. Sugar (too much) seems to be the culprit. He referred me to the below article with a home remedy for fluid replacement recommended by the World Health Organization. Please understand that this is not intended to be a cure-all. Dehydration is serious and should be treated by your doctor. The article follows, along with the orig. link: http://www.medicinenet.com/dehydration/page2.htm

What is the treatment for dehydration? And what are ways of preventing dehydration?

The best way to treat dehydration is to prevent it from occurring. If you suspect excessive fluid loss during and illness, your physician should be notified. Intravenous or oral fluid replacement may be needed, depending on severity of fluid loss. In the 1960's the World Health Organization (WHO) developed an oral solution containing sugar, which improved the absorption of salt/water preparations, saving the lives of many dehydrated persons in remote areas. This solution can be prepared at home by mixing the following:
1. Table Salt - 3/4 teaspoon2. Baking Powder - 1 teaspoon3. Sugar -4 tablespoons4. Orange juice - 1 cup5. Water - 1 quart/liter

This beverage can be taken in small, frequent sips, and is often tolerated in the face of nausea and vomiting. Several commercial preparations are available, but since their composition varies, your physician should be contacted to decide which replacement solution (if any) is best. Changes in the type or amount of fluid replacement may be needed as symptoms improve. Care must be taken to avoid using these solutions improperly.

Food intake should be continued if at all possible, except for high fiber fruits and vegetables. There is controversy regarding ingesting milk products since the ability to absorb milk sugar (lactose) may be reduced. The prior policy of "bowel rest" seems to do more harm than good except in certain circumstances.

Saturday, August 04, 2007

Doctors Post By Marmite

Posted by Marmite on August 02, 2007

REMEMBER 50% of the Doctors graduated in the bottom half of the class.There is ONLY 1 doctor who is BEST in the hospital, State, Country! Then there is always different fields of endeavour.. We go to GI, do you realise that very few specialise in the Pancreas?We go to Surgeons, do you know that very very few specialise in the pancreas.. then there are ones who specialise in roux n y, whipple etc etc. Some are better than others.. Do you know where in the worl dis considered the country of excellence for Pancreas Surgery? India. They have more than 1 billion people, 4 times the pop of the US, so they have more people to operate on.
I have laid in hospital MANY times, A&E way too much and to a lesser extent, wards.I often overhear patients families complaining bitterly that the "doctor SHOULD KNOW .."I have seen people get deathly ill, go to hospital, been admitted, got well, and gone home and NO ONE has any idea what was wrong with them, or how they got better.One lady, on my first trip, couldnt digest food. She could handle "clear soup", cup of black tea or coffee, no problem, but white tea and coffee or cream soup would simply sit there and cause her to bloat. She had a black belt in karate, so she was rather fit and generally healthy. One day they had her scheduled for surgery, she came bac, and the surgeon said "Good news.. it is not cancer!".She was horrified.She asked what it was?? No idea they replied, but it is definitely not cancer!
She got better, and went home, I saw her in hospital a year or two later, same problem and she had lost a lot of weight and condition. I have no idea what has happened since.
You MUST remember that they only perfect diagnostic tool is AUTOPSY, and no one seriously ever wants to go there. Especially not just for a diagnosis.
Celeste and Jerry did 59 dud doctors b4 finding one that worked. You go as far as you have to. You have to put together your MEDICAL TEAM. That includes all of them. Listen to CJ and their experience. Don't stop with anyone who is not the very best, most especially when it comes to surgery.. Panc Surgery is no longer regarded as probably mortal, 30% chance up til the 1990s just from cutting into the pancreas.About that time, I think it was the UK surgeons who decided that only panc accredited surgeons could do scheduled panc surgery. It spread world wide as a std. In emergencies anyone will do what they can to help anyone but if there is panc surgery to do and a panc surgeon is available they lead the team, always!
Again, a great whipple surgeon may be poor on puestow, so check their record. You might wonder how someone gets to be good at something without doing it first, it is the tutor system. If you wanna be a whipple guy, go assist a whipple guy and stand beside him thru all his surgeries, eventually, you will be handed the reigns while he looks over your shoulder.
As the patient or family there of, ASK QUESTIOS. The better the question the greater the respect you develop with your medical practitioner. My GP/PCP at age 60 said he had never seen a case of pancreatitis in General Practice. He vaguely remembered maybe a coupla cases when he was a Reg at the end of his training. he said he had no intimate knowledge, and that he would help but if it were panc related, go to the panc specialist thru the hospital.
When I left my home city to come 200 miles north, for family support, my Panc Surgeon said there was ONLY one guy to talk to here about pancreas here in Welly. Take good advice when it is on offer!
The single most important SECOND thing, after assembling the best medical team you can get no matter what, is to keep the Food & Event diary. This is the greatest diagnostic tool you will ever help with in your particular case. Remember, every panc case is unique and ultimately different to everyone else's! Write down everything you did and ate in the 6-12-24 hours prior to you attack or episode.This is CRITICAL to determining if you contributed to your upset condition. AND you probably did. Many foods do contribute or are even the prime cause of attack. Alcohol is probably the #1, Stress is probably the #1, physical movements are probably the #1, Hot Spice is probably the #1, find out what your #1s are, and avoid them at all costs. Antibiotics were a surprise to me, but they can hurt hurt you. Cold is another one that upsets me, food acid, [apples/tomatoes], all sorts of thiungs will contribute to setting you off. One hospital admission was due to 3 tomatoe sandwiches, I never found this out til 18 months later when a support group meeting tossed this up as a trigger for another person.
I can't speak highly enuff of support groups for pancreatitis. Simply sitting down with other people and telling them how bad that pain was, the horror of the way I live, and they were able to nod sagely and say " I know how that feels"! THAT was special. That is after a long time having A&E doctors and nurses abusing me, frequently, nurses in wards doing the same thru basic ignorance, and lo9tsa people not understanding the condition, me or my particular levels of discomfort with this horrible affliction.
I have never said or posted the word disease. I use affliction, it seems a lot more powerful and nasty. Disease seems to me as a rash, or creeping minor nastiness even if it is severe like leprosy. I don't think it is a BAD enuff word to describe what my pancreas does to me! AFFLICTION, I am afflicted by this damnable medical condition!
Take this seriously, it can kill you. Chronic Pancreatitis will not kill you, but it will destroy your additional organs, liver, kidneys, lungs, heart and lots more. The F&E diary is vital in helping you work out things to do to lower the misery you go thru. It is not a complete solution but it can stop a lot of things starting. As described elsewhere, things like stress can hardly be avoided sometimes. I remember watching the World Trade Centre atrocity unfold live on TV and the stress levels rose, instantly. Simply seeing something as bad as that was translated into pain readily. Stress in everyday life thru family and friends can't be avoided, and that can put you in hospital. Identify every thing in your life which is aggravating your panc condition and then avoid them like the plague.
Talk to family, friends and workmates about your condition and how it effects your everyday life. Tell them things they can do to help or not hurt you, and encourage them to understand you and what exactly you are going thru.
I know my own family never really believed me when I told them what was happening to me and how bad it was. Even when I moved closer to them, they still never really understood, but with time and them doing my total shopping etc, they have come to be my best defenders and they isolate me as much as possible from any and all situations that can hurt me. Namely they deal with all govt departments and hospital administration. They drive me to all doctors visits and come in with me. They help me write out all the questions and points I want to raise and make sure those points are covered as well as writing down answers so I can discuss these with them later if I have missed things.
I no longer function at a high level. I have short term memory problems. I can remember things from school in full detail but can't tell you what happened last week, or even things I agreed to do. I figure this is cos my life is so bland, with no changes, that I don't have points that stand out as different or unique. I only know it is weekend cos the TV programs are different. I don't watch much TV but it is on all the time I am awake, it provides me with human type company while I am alone, which is the way of things except for twice a week. I have a cleaning lady that comes in once a week and my brother and sister come over once to just talk about whatever happens to come up. Life has changed a lot since I was a cab driver dealing with a hundred different people every day!
Stay in control of your life. Do what it takes to monitor you version of this affliction. Inform others about your plight, and ask good questions of your medical team, it will improve your relationship with them.
KEEP your attitude as best you can, positive and be open to suggestions, no matter where they come from. Don't let anyone tell you how to feel or behave, only you can KNOW this. Speak up for yourself, or do what I do, have your family speak for you to insulate yourself from idiots and arseholes, they are everywhere, including hospitals and especially in govt departments.
Have a pain managed day!


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