Pancreatitis Message Board Blog

Dr Sutherland

2007-08-30T07:02:00.000+09:30

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.

Movement of the Pancreas Associated with Change of Posture

2007-08-26T19:06:00.000+09:30

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/

Gastroparesis meds- what do you use?

2007-08-24T22:25:00.000+09:30

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?

2007-08-24T22:18:00.000+09:30

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

2007-08-24T22:15:00.000+09:30

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

2007-08-24T21:59:00.000+09:30

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.

Genetic Testing

2007-08-16T22:10:00.000+09:30

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.

In Reply to: Gastroparesis meds-what do you use?

2007-08-13T19:40:00.000+09:30

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

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

2007-08-07T20:21:00.000+09:30

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.

Doctors Post By Marmite

2007-08-04T19:36:00.000+09:30

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!

This is posted as written by the Author

Liverpool Hospital Link

2007-06-26T00:29:00.000+09:30

Posted by Marmite on June 25, 2007 at 08:59:33:In Reply to: Pancreas - Liverpool Uni posted by Marmite on June 25, 2007 at 08:56
The link posted above should be bookmarked by all of us. Never mind where you are treated, and as I did with Dr Sutherland, you simply email the head sharang and you will get answers and assistance.
You owe it to yourself to have access to the latest in the world of Panc Research and this is one place you can get it..
BOOKMARK IT NOW!!!
Liverpool Uni - Pancreas

Links from Alma

2007-04-11T21:11:00.000+09:30

Posted by Alma on July 22, 2006 at 05:47:04:In Reply to: Lorie...pain 5th vital sign posted by Alma on July 22, 2006:
Lorie,I should have just posted the link below for those needing info on chronic pain. This link will take you to the forms you may want to print out and take to your dr. I keep the one where there is just a drawing of the human body in my wallet along with my medical history. This way all I have to do is hand it to the dr or nurse. It sure helps to have it filled out before seeing a dr or being admitted to the clink because usually when you are in bad pain you have a hard time trying to describe the pain. This scale will provide it for you.http://www2.rpa.net/~lrandall/index.html
Follow Ups:
Posted by Alma on August 05, 2006
Celeste,Do you think we could add this to the link at the bottom of this page and/or to the blog Brett is working with? I think it pertains to some of the issues many of us have and I am also thinking of how it would help this particular organization to be read by other viewers.
http://www.myida.org/index.html
http://www.myida.org/index.html

Posted by Alma on August 11, 2006
I know some of you are trying to get your social security disability. I found these links on the IDA web site and thought you might could use them.
Social Security Disability Advocate - USAdvocates.org - nationwide legal representation for SSA disability issues.http://www.usadvocates.org/
Free 1-on-1 Disability Case Evaluation - Free Attorney Disability Eval. Law Office of Stephanie Joy, Esq. No Fee until you get your benefits. Quicker Results, Higher Success Rate. 1-on-1 with Attorney. All 50 states. Ssdi, SSI.http://www.sojlaw.com/
Free Social Security Disability Help - How to win your social security disability case - The Social Security Disability Resource Site. Have an experienced attorney contact you for a free consultation about your case.http://www.4socialsecuritydisability.com/

Lorie Bledsoe web site

2007-04-11T20:51:00.000+09:30

Posted by Lorie on March 08, 2007
I wanted to let everyone know that my new website is up and running. My Sister KXXXX has built a beautiful site for me to share my Story, journaling, Pictures and Testimonials that my family and friends have written to me. I have been through a lot of kleenex!There are links to my Doctor's and just ton's of information that we keep adding to daily. I want to shout it from the roof tops. If I can get it out there in front of hundreds of people then maybe just maybe I can help someone. I would love to keep anyone from having to endure the pain I have went through. I know you all know and I am sure many of you have the same feelings. My family will journal daily when I have my TP/ICT so each and everyone of you that are interested can follow my journey to hopefully a new life of pain free years. If any of you want to pass it on please do! I have been struggling lately with anxiety and a lot of pain and nausea. The thing that keeps me going right now is the hope of a new life and sharing my journey so I can be a voice for the people that are unable to. The support of friends and family means the world to me right now! Thank You for that! Lorie http://www.supportloriebledsoe.com/

New System more precise than ERCP?

2007-04-11T20:47:00.000+09:30

New Visualization System Found to Be More Precise than ERCP
Researchers reported at the DDW (Digestive Disease Week) meeting in Los Angeles, that direct visualization with a device called SpyGlass™ altered their diagnosis or treatment strategy with most patients who had been previously examined with ERCP.Data shows that up to 30% of diagnostic ERCP are inconclusive, potentially creating the need for further testing. ‘Direct visualization significantly improves the chances of accurately diagnosing and treating a patient in one procedure, thus achieving the full potential of ERCP’, stated lead investigator Yang K. Chen, MD, from the University at Colorado at Denver and Health Sciences Center. Both bench simulation and animal testing showed that the SpyGlass system to be effective for access, direct visualization and biopsy in all bile duct quadrants. Furthermore, this procedure can be performed by a single operator, as compared to conventional systems where two operators are required. In this investigator initiated first human use experience and bench simulation study, the researchers used the SpyGlass system to examine and treat 22 patients with various disorders. According to DDW co-presenter Douglas Pleskow, MD, Colon Cancer Center, Beth Israel Deaconess Medical Center, Boston, Mass., ‘the use of SpyGlass altered the initial ERCP impression and ultimately changed patient treatment strategy in 19 patients.’ To overcome the limitations of conventional ERCP, this new system uses a miniature 6,000-pixel fiber optic SpyGlass probe that attaches to the camera head. The probe is inserted through a single-use access and delivery catheter that can be steered in four directions to access and inspect all four quadrants of the treatment area. The system attaches directly to a standard duodenal scope. The SpyGlass system is manufactured by Boston Scientific Corporation. The company’s Senior Vice President, Steve Moreci, summed up the results by saying that ‘These studies indicate that the SpyGlass Direct Visualization System has the potential to redefine how ERCP is performed and to potentially help physicians obtain a more accurate diagnosis quickly.’

Dr's Oath..First Do No Harm

2007-04-11T20:44:00.000+09:30

"The D,R fundamental role is to alleviate the distress of his or her fellow men,and no motive, whether personal collective, or political,shall prevail against this higher purpose"Declaration of Tokyo, World Medical Association (1975)Physicians and other medical professionals swear to do no harm.

Port-A-Cath

2007-04-06T11:00:00.000+09:30

On the 25th of June I am going to have a Port-A-Cath inserted in my spine. Below is the information and Diagrams that I have received in preparation for this. What this will enable me to do is deliver very small doses of lignocaine or narcotic medication directly to my spine therefore eliminating my pain. I will have to inject every 4 or so hours . This will then let me wean myself off my narcotic medication and control my pain during this process. The Dr’s believe if I then stay off the narcotic medication for a little while I will be able to restart the same medication and get a much better result or a significantly lower dose. It will be as if I had never taken the drug before. They may leave the port in place for as long as it is working and causing no problems. Up to 5 years.

My Pain is my prisoner

2006-08-22T21:10:00.000+09:30

My pain is my prisoner, it's not what I want
It makes me to lie down between hospital sheets
It destroyeth my soul:
It loses me in the paths of sickness, I’m sick of its name Even tho I walk down the hospital corridors is till fear evil,
Tho my drip is with me its pole and its bad don’t comfort me
They prepare others tables in the presence of my nausea
They assault my body with drugs, my patience runs out.
Surely illness and despair will leave me and I will dwell in this house of sickness no MORE!!

This was posted on the PMB with a request to find out who the orginal Author was. So if you can help then please feel free to post a comment. Thanks for your help.

What does S.O.D. Stand for?

2006-08-02T22:36:00.000+09:30

In Reply to: ps. what does sod stand for? posted by jeff on July 24, 2006 at

Sphincter of oddi disfunction.. its also on jerrys blog.. I'll put the pic here and then paste the info in this post**************************************************

This is a picture that shows the sphincter of oddi. the main pancreatic duct and bile duct from the liver both converge and their liquids are released via the sphincter. The main pancreatic duct will back up with activated enzymes and they will eat and destroy all along the length of the pancreas. In the torso diagram, where the head of the pancreas is (torsos right side) Jerry has a knot that protrudes out of his abdomen. We were todl that the pancreas is swelling so large that it pushes out from under the stomach and that is what is causing the bulge.*******************************************

ps the bulge is gone and has not returned! so it was the pancreas and NOT a food bolus!

Insurance Help Sites

2006-08-02T22:34:00.000+09:30

Posted by cj on July 10, 2006 at 14:49:28:In Reply to: no insurance and help?
Patient assistance programs-helpingpatients.org/
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http://www.3m.com/us/healthcare/pha...ssistance.jhtml
http://sis.nlm.nih.gov/hotlines/
http://coveringkidsandfamilies.org/communications/bts/
http://www.freemedicineprogram.com/drug/ELDER+TONIC/
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http://www.astrazeneca-us.com/content/drugAssistance/
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http://www.lillyanswers.com/
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Bristol Stool Scale

2006-08-02T22:30:00.000+09:30

Bristol Stool ScaleFrom Wikipedia, the free encyclopediaYou have new messages (last change).Jump to: navigation, search

The Bristol Stool Scale or Bristol Stool Chart is a medical aid designed to classify the faeces form into seven groups. It was developed by Heaton and Lewis at the University of Bristol and was first published in the journal Scand J Gastroenterol in 1997. Because the form of the stool depends on the time it spends in the colon, there is a correlation between the colonic transit time and the stool type.
The seven types of stool are:

Type 1: Separate hard lumps, like nuts (hard to pass)
Type 2: Sausage-shaped, but lumpy
Type 3: Like a sausage but with cracks on its surface
Type 4: Like a sausage or snake, smooth and soft
Type 5: Soft blobs with clear cut edges (passed easily)
Type 6: Fluffy pieces with ragged edges, a mushy stool
Type 7: Watery, no solid pieces (entirely liquid)

Types 1 and 2 indicate constipation, with 3 and 4 being the "ideal stools" especially the latter, as they are the easiest to pass. 5-7 being further tending towards diarrhoea.
[edit]ReferencesConstipation Management and Nurse Prescribing: The importance of developing a concordant approach PDF Faecal incontinence and constipation PDF [edit]External linksThe Bristol Stool Scale from Medscape.com Information from Solvay Pharmaceuticals Childhood Constipation Retrieved from "http://en.wikipedia.org/wiki/Bristol_Stool_Scale"Categories: General practice | Gastroenterology

Ambry Test

2006-08-02T22:28:00.000+09:30

Posted by cj on July 20, 2006 at 16:10:14
http://www.ambrygen.com/reports/Pancreatitis%20Sales%20Aid%205-06.pdf

The Ambry Test : PancreatitisPancreatitis is a serious problem with asignificant genetic component.Pancreatitis accounts for 87,000 hospitalizationsper year in the US.1 Chronic pancreatitis patientsface a 26-fold increased risk of pancreatic cancer,and for those with hereditary pancreatitis, the riskis 50-fold with approximately 40% developingpancreatic cancer by age 70.2Normal exocrine pancreatic function depends on adelicate balance of enzyme activation andinhibition which can be affected by multipleenvironmental and genetic factors. Hereditarypancreatitis has been linked to mutations in thePRSS1 gene. Study of idiopathic chronic andrecurrent acute pancreatitis demonstrates thatmutations in three genes – PRSS1, SPINK1, andCFTR – predispose to pancreatitis.3Due to the cumulative contribution of three genesin both dominant and recessive patterns, a patientmay have genetically-determined pancreatitis evenif family history is negative.Ambry Genetics offers the world’s onlycomprehensive genetic test for pancreatitis.To help determine etiology and suggestappropriate treatments, Ambry Genetics offersanalysis of all coding regions of the CFTR, PRSS1,and SPINK1 genes in The Ambry Test: PancreatitisAMPLIFIED™. This test also analyzes the CFTRgene for gross deletions and duplications, whenindicated, providing a detection rate ofapproximately 99% for each gene. The panel isalso available without CFTR deletion/duplicationanalysis (The Ambry Test: Pancreatitis, CFdetection rate 97-98%), and each test is availableseparately.100 Columbia #200 | Aliso Viejo, CA 92656 | 949 900 5500fax 949 900 5501 | toll free 866 262 7943 |
www.ambrygen.com|

Pancreatitis1 in 4 patients tests positive for at least onesignificant genetic mutation.Mutations in three genes predispose to chronicand recurrent acute pancreatitis:• CFTR – cystic fibrosis transmembraneconductance regulator• PRSS1 – cationic trypsinogen• SPINK1 – serine protease inbitor, Kazal type 1Genetic testing for pancreatitis can help you:• Avoid repeated diagnostic testing• Provide targeted therapy• Address increased cancer risk in geneticallydeterminedpancreatitis• Help your patient understand his condition andincrease compliance• Communicate inheritance risks tofamily membersNo other test can identifymore mutations thanThe Ambry Test:Pancreatitis AMPLIFIEDGet started with Ambry Genetics today.Sample submission kits are available atno charge. Please call 866-262-7943 or visitour website to obtain more information andall necessary forms.™100 Columbia #200 | Aliso Viejo, CA 92656 | 949 900 5500fax 949 900 5501 | toll free 866 262 7943 | www.ambrygen.com|

Pancreatitis• In the entire patient set, 49.1% (116/236) carriedat least one mutation.• 11.0% (26/236) had a form of CF confirmed by2 CF mutations. An additional 22.0% (52/236)had one CF mutation.• 8.9% (21/236) had mutations in more than one gene.• Only 4.2% (10/236) patients had PRSS1mutations only.• Approximately 1/4 patients (23.7%, 56/256) havemutations with a clear causative component(defined as presence of 2 CF mutations and/orknown deleterious PRSS1 or SPINK1 mutations).83891, 83894, 83898,83903, 83904, 83909,839123-5 WeeksFull gene mutation scanning is performed by modified TemporalTemperature Gradient Electrophoresis (mTTGE). All sequencevariations detected by mTTGE are identified by double-strandedautomated sequencing. If indicated, CFTR gross deletion /duplication testing is performed by MLPA (MRC Holland).Blood: 5cc peripheral blood in purple-top EDTA (preferred) oryellow top ACD. Store at 2-8° C up to 96 hours prior toshipping. Do not freeze. Ship at room temperature.CPT CodesTurn-Around-TimeMethodSpecimenRequirements1 Yakshe P. Pancreatitis, chronic. emedicine [online resource]. Available at: http://www.emedicine.com/MED/topic1721.htm. Last update July 2005.2 Erickson RA. Pancreatic cancer. emedicine [online resource]. Available at: http://www.emedicine.com/MED/topic1712.htm. Last update Dec 2005.3 Etemad B, Whitcomb DC. Gastroenterology. 2001;120:682-707.4 Whitcomb DC.US Gastro Review. 2006;56-58, and personal communication.© 2006 Ambry Genetics. All rights reserved. P0506-09-003-MKG-00.PANCREATITIS PANEL PANCREATITIS PANEL AMPLIFIED83891, 83894, 83898, 83900,83901, 83903, 83904, 83909,839124-6 Weeks1 in 4 patients has at least onesignificant mutation.In a series of patients with chronic or recurrentacute pancreatitis, The Ambry Test: Pancreatitisdetected at least one mutation in 49.1% (116/236).Though patients known to have cystic fibrosis (CF)were excluded from this series, 11.0% (26/236) werefound to have a form of CF confirmed with at leasttwo CFTR mutations. Nearly as many patients(8.9%, 21/236) had mutations in more thanone gene.Using a stricter definition of clinical significance aspresence of known deleterious mutations in PRSS1or SPINK1, and/or two CF mutations, approximatelyone in four patients (23.7%, 56/236) has a causativegenetic component to their pancreatitis.Genetic testing results can help youmanage your patient.As mutations in different genes affect differentsteps of trypsin activation and inhibition, genetictesting can suggest treatments targeted to apatient’s particular defect. For example, PRSS1mutations may lead to premature trypsinogenactivation through altered sensitivity to calcium.Preventive measures could include various steps tominimize stimulation of the acinar cells and assistcalcium regulation.4 CFTR mutations impairpancreatic duct flushing, so treatments could focuson stimulating the pancreas and maximizing flowthrough the duct.4Identifying patients with mutations allowsappropriately increased cancer surveillance.Knowledge of contributory mutations explains thedisease to the patient, reinforces understanding ofits chronic nature, and affirms the importance ofcompliance with dietary and lifestyle modifications.Further, family members may be tested andcounseled to minimize their risk of developingchronic pancreatitis.Mutation distribution in 236 patients testedwith The Ambry Test: Pancreatitits

The Ambry Test : PancreatitisPancreatitis is a serious problem with asignificant genetic component.Pancreatitis accounts for 87,000 hospitalizationsper year in the US.1 Chronic pancreatitis patientsface a 26-fold increased risk of pancreatic cancer,and for those with hereditary pancreatitis, the riskis 50-fold with approximately 40% developingpancreatic cancer by age 70.2Normal exocrine pancreatic function depends on adelicate balance of enzyme activation andinhibition which can be affected by multipleenvironmental and genetic factors. Hereditarypancreatitis has been linked to mutations in thePRSS1 gene. Study of idiopathic chronic andrecurrent acute pancreatitis demonstrates thatmutations in three genes – PRSS1, SPINK1, andCFTR – predispose to pancreatitis.3Due to the cumulative contribution of three genesin both dominant and recessive patterns, a patientmay have genetically-determined pancreatitis evenif family history is negative.Ambry Genetics offers the world’s onlycomprehensive genetic test for pancreatitis.To help determine etiology and suggestappropriate treatments, Ambry Genetics offersanalysis of all coding regions of the CFTR, PRSS1,and SPINK1 genes in The Ambry Test: PancreatitisAMPLIFIED™. This test also analyzes the CFTRgene for gross deletions and duplications, whenindicated, providing a detection rate ofapproximately 99% for each gene. The panel isalso available without CFTR deletion/duplicationanalysis (The Ambry Test: Pancreatitis, CFdetection rate 97-98%), and each test is availableseparately.100 Columbia #200 | Aliso Viejo, CA 92656 | 949 900 5500fax 949 900 5501 | toll free 866 262 7943 | www.ambrygen.com| Pancreatitis

1 in 4 patients tests positive for at least onesignificant genetic mutation.Mutations in three genes predispose to chronicand recurrent acute pancreatitis:• CFTR – cystic fibrosis transmembraneconductance regulator• PRSS1 – cationic trypsinogen• SPINK1 – serine protease inbitor, Kazal type 1Genetic testing for pancreatitis can help you:• Avoid repeated diagnostic testing• Provide targeted therapy• Address increased cancer risk in geneticallydeterminedpancreatitis• Help your patient understand his condition andincrease compliance• Communicate inheritance risks tofamily membersNo other test can identifymore mutations thanThe Ambry Test:Pancreatitis AMPLIFIEDGet started with Ambry Genetics today.Sample submission kits are available atno charge. Please call 866-262-7943 or visitour website to obtain more information andall necessary forms.™100 Columbia #200 | Aliso Viejo, CA 92656 | 949 900 5500fax 949 900 5501 | toll free 866 262 7943 | www.ambrygen.com| Pancreatitis•

In the entire patient set, 49.1% (116/236) carriedat least one mutation.• 11.0% (26/236) had a form of CF confirmed by2 CF mutations. An additional 22.0% (52/236)had one CF mutation.• 8.9% (21/236) had mutations in more than one gene.• Only 4.2% (10/236) patients had PRSS1mutations only.• Approximately 1/4 patients (23.7%, 56/256) havemutations with a clear causative component(defined as presence of 2 CF mutations and/orknown deleterious PRSS1 or SPINK1 mutations).83891, 83894, 83898,83903, 83904, 83909,839123-5 WeeksFull gene mutation scanning is performed by modified TemporalTemperature Gradient Electrophoresis (mTTGE). All sequencevariations detected by mTTGE are identified by double-strandedautomated sequencing. If indicated, CFTR gross deletion /duplication testing is performed by MLPA (MRC Holland).Blood: 5cc peripheral blood in purple-top EDTA (preferred) oryellow top ACD. Store at 2-8° C up to 96 hours prior toshipping. Do not freeze. Ship at room temperature.CPT CodesTurn-Around-TimeMethodSpecimenRequirements1 Yakshe P. Pancreatitis, chronic. emedicine [online resource]. Available at: http://www.emedicine.com/MED/topic1721.htm. Last update July 2005.2 Erickson RA. Pancreatic cancer. emedicine [online resource]. Available at: http://www.emedicine.com/MED/topic1712.htm. Last update Dec 2005.3 Etemad B, Whitcomb DC. Gastroenterology. 2001;120:682-707.4 Whitcomb DC.US Gastro Review. 2006;56-58, and personal communication.© 2006 Ambry Genetics. All rights reserved. P0506-09-003-MKG-00.PANCREATITIS PANEL PANCREATITIS PANEL AMPLIFIED83891, 83894, 83898, 83900,83901, 83903, 83904, 83909,839124-6 Weeks

1 in 4 patients has at least onesignificant mutation.In a series of patients with chronic or recurrentacute pancreatitis, The Ambry Test: Pancreatitisdetected at least one mutation in 49.1% (116/236).Though patients known to have cystic fibrosis (CF)were excluded from this series, 11.0% (26/236) werefound to have a form of CF confirmed with at leasttwo CFTR mutations. Nearly as many patients(8.9%, 21/236) had mutations in more thanone gene.Using a stricter definition of clinical significance aspresence of known deleterious mutations in PRSS1or SPINK1, and/or two CF mutations, approximatelyone in four patients (23.7%, 56/236) has a causativegenetic component to their pancreatitis.Genetic testing results can help youmanage your patient.As mutations in different genes affect differentsteps of trypsin activation and inhibition, genetictesting can suggest treatments targeted to apatient’s particular defect. For example, PRSS1mutations may lead to premature trypsinogenactivation through altered sensitivity to calcium.Preventive measures could include various steps tominimize stimulation of the acinar cells and assistcalcium regulation.4 CFTR mutations impairpancreatic duct flushing, so treatments could focuson stimulating the pancreas and maximizing flowthrough the duct.4Identifying patients with mutations allowsappropriately increased cancer surveillance.Knowledge of contributory mutations explains thedisease to the patient, reinforces understanding ofits chronic nature, and affirms the importance ofcompliance with dietary and lifestyle modifications.Further, family members may be tested andcounseled to minimize their risk of developingchronic pancreatitis.Mutation distribution in 236 patients testedwith The Ambry Test: Pancreatitits

Celiac Plexus Block

2006-08-02T22:16:00.000+09:30

In Reply to: Celiac Plexus Nerve Blocks posted by Robin H. on August 01, 2006 at 10:42:48:
(image placeholder)
I knew someone on here had had something diff done. Thats why i told jeff, someone else will pipe up with info. also i found this neat page!!
*****************************************************ROUND TABLE

Article in PDF format - JOP Home page
JOP. J Pancreas (Online) 2004; 5(4):315-321.
Celiac Plexus Neurolysis
Paolo Giorgio Arcidiacono, Marzia Rossi
Diagnostic and Therapeutic Endosonography Unit, Division of Gastroenterology and Gastrointestinal Endoscopy, Vita-Salute San Raffaele University - San Raffaele Hospital. Milan, Italy
Introduction
Pancreatic cancer is the tenth most common malignancy and the fourth cause of cancer-related death in Western countries. Because 5-year survival in referral centers is less than 30%, clinical management of most patients involves palliation of the symptoms of which 90% are weight loss, jaundice, and pain.
While jaundice related to biliary obstruction can be palliated by means of endoscopic therapy or surgery, pancreatic pain is often difficult to control.
Initial therapy with non-steroid anti-inflammatory agents (NSAIDs) is often rapidly overwhelmed by pain and necessitates being associated with opioid administration.
Although opioids effectively relieve pain, they are associated with many different collateral effects, such as dry mouth, constipation, nausea, vomiting, drowsiness and delirium, which can determine a great decrease in quality of life and may also impair the immune function. Pancreatic pain is also quite common in patients with chronic pancreatitis and, in this case, pain has a multi-factorial etiology; for this reason, prolonged drug therapy is related to an increased risk of narcotic-dependence [1].
Celiac plexus neurolysis (CPN) is a chemical splanchnicectomy of the celiac plexus; its goal is to ablate the efferent nerve fibres which transmit pain from the intra-abdominal viscera.
Although the terms "celiac plexus" and "splanchnic nerves" are often used interchangeably, these are anatomically distinct structures.
The splanchnic nerves are located above the diaphragm (retro-crural) and are typically anterior to the 12th thoracic vertebra; on the other hand, the celiac plexus is situated below the diaphragm (ante-crural), surrounding the basis of the celiac trunk. This plexus is composed of a dense network of ganglia and interconnecting fibres (Figure 1).
Figure 1. The celiac plexus.
The ganglia vary in number (1-5), size (diameter 0.5-4.5 cm), and location (T12-L2), but, independently on their size, the ganglia cannot be visualized as distinct structures by any kind of imaging modality.
The celiac plexus transmits pain sensation originating from the pancreas and most of the abdominal viscera except for the left colon, rectum and pelvic organs.
Stimuli reach the thalamus and the cortex of the brain, leading to pain sensation. On the contrary, some descending inhibitory mechanisms may also modulate the ascending pain information.
The CPN technique was first described by Kappis et al. in 1919 [2]; since then, a number of modifications have been proposed and introduced in a clinical setting in an attempt to improve the accuracy of needle placement and pain relief while reducing procedure-related complications.
Nowadays, CPN is most commonly used to palliate patients suffering from pain due to pancreatic cancer and chronic pancreatitis; it can be performed using different approaches either percutaneously, surgically or under EUS guidance. Until the 1990s, the most common of the above was surely the percutaneous route, injecting absolute alcohol into the celiac plexus under fluoroscopy or CT guidance.
Different studies have reported data on safety, accuracy in reaching the right site of injection and efficacy in decreasing pain due to different diseases by means of CT-guided CPN.
Some authors described 28 cases of CPN performed under CT guidance in patients having neoplasms originating in the pancreas (n=10), stomach (n=8), bile ducts (n=5), liver (n=3), right colon (n=1) and kidney (n=1) [3]. The study showed that this procedure is safe and efficient in controlling pain [3].
Unfortunately, the CT CPN approach is usually posterior and, for this reason, cases of paraplegia have been reported caused by the puncture of the nervous radix at the time of the introduction of the needle during the procedure [4].
Endoscopic ultrasonography (EUS) is a relatively new imaging technique which couples a high frequency ultrasound probe with an oblique viewing endoscopic instrument. This combination allows the endoscopist to obtain a perfect evaluation of the pancreatic parenchyma and surrounding structures, not least, the aorta and celiac trunk. This imaging modality has achieved wide acceptance as the technique of choice for the evaluation of pancreatic disease, diagnosis and staging of pancreatic cancer, diagnosis of idiopathic pancreatitis and the evidencing of neuro-endocrine neoplasms.
At the beginning of EUS, instruments were provided by radial scanning probes; this means that the scanning plane of these probes was transversal, that is, perpendicular to the longitudinal axis of the endoscopic instrument.
This probe orientation absolutely limited the possibility of these instruments performing EUS guided diagnostic or therapeutic procedures, due to the inability of the probe to follow, under real time guidance, the route of a needle device from the orifice of the working channel of the EUS instrument to a target lesion located either inside the gut wall or, as for CPN, outside the gut wall. In early 1990s, there was a technical revolution in EUS instrumentation; in fact, a longitudinal echoendoscope was presented.
This instrument was made with an electronic convex high frequency probe having a longitudinal scanning plane; this means that the scanning plane was on the same longitudinal axis as the endoscope and, more importantly, on the same axis of the working channel.
This innovation has opened the field of operative EUS, allowing the possibility of following, under real time guidance, any kind of device passed throughout the working channel to reach a target lesion.
Since that time, EUS has been tested in this new operative setting for many reasons, mainly the cytological analysis of tumors and, more recently, it has been applied in the treatment of pain in patients with chronic pancreatitis or pancreatic cancer by injecting neurolytic agents in the area of the celiac plexus.
Although many studies demonstrate that celiac plexus neurolysis effectively controls pancreatic cancer pain, up to 1% of patients undergoing percutaneous CPN may develop serious complications, including lower extremity weakness, paresthesias, including epidural anesthesia, lumbar puncture and pneumothorax.
In theory, EUS CPN is safer than posterior percutaneous techniques because EUS allows direct access to the celiac plexus without risk to the vital spinal nerves, the diaphragm or the spinal arteries.
Procedure
EUS-guided celiac plexus neurolysis (EUS CPN) is usually combined with the biopsy of a pancreatic primary lesion for diagnostic and staging purposes. It is performed with a linear array echoendoscope (Figure 2).
Figure 2. Linear array echoendoscope.
With these instruments, it is possible to follow, under EUS real time guidance, the route of the needle through the pancreatic lesion.
Informed consent is obtained with specific attention to complications associated with CPN and EUS guided fine needle aspiration (FNA) of pancreatic lesions. The procedure is performed under deep sedation under the supervision of an anesthesiologist. The patient lays on left lateral decubitus and his/her vital parameters are monitored.
Under direct endoscopic view, the linear EUS instrument is introduced into the stomach to reach the lesser curve in the sub-cardiac area. In this position, the probe is lightly pressed against the gastric wall to obtain a good coupling and a good view of surrounding structures. At this site, it is easy to identify the aorta under the diaphragm which appears as an anechoic tube structure in a longitudinal plane and the origin of the celiac axis is seen beside this. Color Doppler can confirm the vascular landmarks (Figures 3 and 4).
Figure 3. Monochrome visualization of the celiac trunk.
Figure 4. Color Doppler visualization of the celiac trunk.
As previously emphasized, the celiac plexus is not identified as a discrete structure but is located based on its position relative to the celiac trunk.
Two different treatment procedures have been described to perform EUS CPN depending on the device used to perform alcohol injection.
The first technique described uses a standard 22 gauge needle used for all the biopsy procedures under EUS guidance (Figure 5); this is a cutting needle with a removable inner sheet occluding a single hole at the needle tip. For this reason, it is necessary to perform two injections of alcohol at both sides of the trunk in order to obtain an adequate injection of alcohol at both sides of the celiac trunk.
Figure 5. Standard 22 gauge needles.
The second procedure, which is actually more diffused due to its rapidity, uses a new needle (Figure 6) properly designed for this procedure (EUS 20 CPN, Wilson Cook, Winston-Salem, NC, USA); it is a 20 gauge needle with a penetrating tip closed and with some lateral holes which allow a radial diffusion of alcohol to both sides of the origin of the celiac axis with a single injection.
Figure 6. EUS 20 CPN (Wilson Cook, Winston-Salem, NC, USA) needle.
Once the origin of the celiac trunk is located from the sub-cardiac position, the needle (whichever used) is passed through and fixed to the celiac trunk by a luer-lock. Then, under real time control, the needle is released and pushed out from the working channel to trans-pass the gastric posterior wall and is immediately inserted adjacent to the celiac trunk.
At this phase, the two procedures differ slightly, considering the needle position with respect to the celiac trunk; in the first procedure, due to the fact that the needle has only one hole and cannot spray alcohol, the needle tip is positioned by one side of the trunk originating from the aorta and, after having completed the injection, it must be pulled back slightly and again inserted on the other side of the trunk to carry out another injection.
In the second technique, the spraying possibility given by the EUS 20 CPN needle allows the endosonographer to put the needle tip anterior to the basis of the origin of the celiac axis and to carry out only one injection (Figure 7).
Figure 7. EUS image of the needle at base of the celiac trunk.
The injection time is identical for both devices used. When the needle tip is in place, the inner sheet is removed and an aspiration test is performed to rule out vessel penetration before injection.
Then, 3-6 mL of a local analgesic, usually bupivacaine 0.25-0.75%, is injected first followed by 15-20 mL of a neurolytic agent (98%) dehydrate alcohol (Figure 8).
Figure 8. EUS image of lidocaine injection.
The alcohol injection produces an echogenic cloud obscuring the aorta and celiac axis (Figure 9).
Figure 9. EUS image of alcohol injection showing an echogenic cloud obscuring aorta and celiac axis.
In chronic pancreatitis patients, some Authors prefer to use steroids (10 mL or 80 mg (6 mL) triamcinolone) instead of alcohol.
However, in chronic pancreatitis, most results are obtained with alcohol and when traditional techniques were used.
The EUS CPN procedure usually lasts approximately 15 minutes and, during the procedure, arterial pressure has to be monitored because the alcohol injection may produce hypotension and it is necessary to infuse saline solution.
Results
Currently, there are few data about CPN under EUS guidance. However, the results are comparable to other conventional methods used to relieve pancreatic pain with neurolytic agent injections.
The safety and efficacy of EUS CPN has previously been demonstrated as relieving pancreatic pain in a cohort of 25 patients with pancreatic cancer followed for 12 weeks and 5 patients with other intra-abdominal malignant neoplasms [5]. These studies showed a significant decrease of pain at 2, 4, 8 and 12 weeks after EUS CPN.
About 80% of the patients also benefited in a long-term observation (a mean follow up-of 10 weeks) [5]. Other Authors described 58 patients treated in order to palliate pain due to non-operable pancreatic cancer. A short-term decrease of pain was seen in 78% of the patients but the control of pain decreased in 30% at 12 weeks.
Of particular interest is the evidence, reported by Gunaratnam et al. in the widest population reported to have been treated using this modality, that, if the treatment is associated with chemoradiation or chemotherapy, the decrease in the pain score was significantly higher as compared to patients who did not undergo any additional therapy [6] (Figure 10).
Figure 10. Decrease of the pain score according to different treatments. (N Gunaratnam et al. [6], modified).
Up to now, the real role of EUS CPN in the treatment of pain related to chronic pancreatitis is not so clear, lacking enough comparative data comparing EUS CPN and other modalities of treating such multifactorial pain.
Only two studies [7, 8] have tested EUS CPN in this setting; in 90 patients steroids were injected during EUS CPN and a beneficial effect was observed after 7 days in only 55% [7]. Furthermore, in the follow-up of these patients, only 25% still showed a significant decrease in the pain score after 12 weeks [7].
Many authors believe that the difference in results between patients with pancreatic cancer or chronic pancreatitis probably depends on the origin of the pain which can be considered only due to the nervous growing of the tumor in pancreatic cancer and which is multifactorial, with a great psychological impact, in chronic pancreatitis.
Another study described 22 cases of CPN (10 EUS CPN and 12 CT CPN) which showed the benefit in 40% at 8 weeks under EUS guidance (30% at 24 weeks) and in 25% under CT guidance. But the Authors concluded that the number of patients was too limited [8].
There are only a few complications related to the procedure and they are described as only transitory [3]. Orthostatic hypotension or a transient diarrhea may frequently be described.
The infusion of liquid can contrast the hypotension, while the diarrhea is generally auto-limiting and does not exceed 24 hours. Only a few cases of chronic diarrhea have been described; other complications are: peri-pancreatic abscess, reversible paraparesis and a pseudo alcohol-induced aneurysm [9, 10, 11]. To prevent the abscess, it is important to carry out antibiotic prophylaxis.
Conclusions
Celiac plexus neurolysis during EUS appears to be a safe technique, without complications. It seems to control neoplastic pancreatic pain in a short time in about 90% of cases and in a long time in about 30%.
In the management of chronic pancreatitis pain, the role of EUS CPN is not so clear and only 50% of patients have a good reduction of pain within a short period of time. However, only 10% seem to show a benefit at 24 weeks. EUS CPN results seem to be comparable to the results obtained with the other procedures, although the numbers are still too low. An important advantage is that EUS CPN may be performed during bioptic staging of pancreatic cancer [12].
It is also not very clear if there is the possibility of performing more than one procedure of neurolysis.
In summary, EUS CPN is safe and effective for the palliation of patients with pain caused by unresectable pancreatic cancer. Chemotherapy with and without radiotherapy also significantly decreased pain scores.
In addition, the proximity of the posterior lesser curve of the stomach to the celiac plexus, the use of continuous real time visualization of the target area and the availability of the Doppler to assess the vasculature all facilitate accurate needle placement.
CPN under EUS guidance requires further investigation in order to identify the advantages of this approach over conventional percutaneous techniques. The ability to perform the procedure in conjunction with tumor staging and FNA may streamline the care of these patients. The use of EUS CPN earlier in the course of pancreatic cancer to alleviate pain should be encouraged.
References
Levy MJ, Wiersema MJ. EUS-guided celiac plexus neurolysis and celiac plexus block. Gastrointest Endosc 2003; 57:923-9. [More details]
Kappis M. Sensibilitat und lokale Anasthesie im chirurgischen Gebiet der Bauchhohle mit besonderer Berucksichtigung der splanchnicus-Aasthesie. Beitrage zur klinischen Chirurgie 1919; 115:161-75. [More details]
Lee JM. CT-guided celiac plexus block for intractable abdominal pain. J Korean Med Sci 2000; 15:173-8. [More details]
Eisenberg E, Carr DB, Chalmers CT. Neurolytic celiac plexus block for treatment of cancer pain: a meta-analysis. Anesth Analg 1995; 80:290-5. [More details]
Wiersema MJ, Wiersema LM. Endosonography-guided celiac plexus neurolysis. Gastrointest Endosc1996; 44:656-62. [More details]
Gunaratnam NT, Sarma AV, Norton ID, Wiersema MJ. A prospective study of EUS-guided celiac plexus neurolysis for pancreatic cancer pain. Gastrointest Endosc 2001; 54:316-24. [More details]
Gress F, Schmitt C, Sherman S, Ciaccia D, Ikenberry S, Lehman G. Endoscopic ultrasound-guided celiac plexus block for managing abdominal pain associated with chronic pancreatitis: a prospective single center experience. Am J Gastroenterol 2001; 96:409-16. [More details]
Gress F, Schmitt C, Sherman S, Ikenberry S, Lehman G. A prospective randomized comparison of endoscopic ultrasound- and computed tomography-guided celiac plexus block for managing chronic pancreatitis pain. Am J Gastroentero. 1999; 94:900-5. [More details]
Chan VW. Chronic diarrhea: an uncommon side effect of celiac plexus block. Anesth Analg 1996; 82:205-7. [More details]
Navarro-Martinez J, Montes A, Comps O, Sitges-Serra A. Retroperitoneal abscess after neurolytic celiac plexus block from the anterior approach. Reg Anesth Pain Med 2003; 28:528-30. [More details]
Kumar A, Tripathi SS, Dhar D, Bhattacharya A. A case of reversible paraparesis following celiac plexus block. Reg Anesth Pain Med 2001; 26:75-8. [More details]
Varadarajulu S, Wallace MB. Applications of endoscopic ultrasonography in pancreatic cancer. Cancer Control 2004; 11:15-22. [More details]
Article in PDF format
--------------------------------------------------------------------------------
Keywords Celiac Plexus /innervation; Endosonography; Pain; Pancreatic Neoplasms
Abbreviations CPN: celiac plexus neurolysis
CorrespondencePaolo Giorgio ArcidiaconoDivision of Gastroenterology and Gastrointestinal EndoscopyUniversity Vita-Salute San RaffaeleIRCCS San Raffaele HospitalVia Olgettina, 6020132 MilanoItalyPhone: +39-02.2643.2145Fax: +39-02.215.2559E-mail address: arcidiacono.paologiorgio@hsr.it
JOP Home page

http://www.joplink.net/prev/200407/26.html

Blood Work Questions

2006-08-02T22:10:00.000+09:30

Posted by cj on July 19, 2006 at 12:51:57:
In Reply to: blood work question?? posted by jeff

Lab Studies:
Blood tests
**Elevations of serum amylase and lipase are found only during acute attacks of pancreatitis, usually early in the course of the disease**In the later stages of chronic pancreatitis, atrophy of the pancreatic parenchyma can result in serum
enzyme levels within the reference range, even during acute attacks of pain.
While low concentrations of serum trypsin are relatively specific for advanced chronic pancreatitis, they are not sensitive enough to be helpful in most patients with mild-to-moderate disease.
Laboratory studies to identify causative factors include serum calcium and triglyceride levels.
When common etiologies are not found, research protocols are available to test for genetic mutations in cationic trypsinogen and CFTR.
Fecal tests
Because maldigestion and malabsorption do not occur until more than 90% of the pancreas has been destroyed, steatorrhea is a manifestation of advanced chronic pancreatitis, and neither qualitative nor quantitative fecal fat analysis can detect early disease.
Assays of fecal chymotrypsin and human pancreatic elastase 1 have the same limitations but are useful in confirming advanced chronic pancreatitis with exocrine insufficiency.
Pancreatic function tests
Direct tests: These tests are the most sensitive and can be used to detect chronic pancreatitis at its earliest stage; however, they are somewhat invasive, labor intensive, and expensive.

Determination in duodenal aspirates: Intubation of the duodenum usually is performed with a Dreiling tube, which allows for separate aspiration of gastric and duodenal contents. The methodology varies depending on the specific laboratory; however, the authors generally use exogenous secretin with cerulein or cholecystokinin to achieve maximal stimulation of the pancreas. The output of pancreatic bicarbonate, protease, amylase, and lipase then is measured in the duodenal aspirates. This test currently only is available in specialized centers. While the greatest sensitivity can be obtained in prolonged infusions of secretagogue to uncover a decreased pancreatic secretory reserve, it is impractical for general clinical use.

Determination in pancreatic juice: This test generally is performed in conjunction with an endoscopic retrograde cholangiopancreatography (ERCP). The pancreatic duct is freely cannulated, an exogenous secretagogue is administered as above, and the pancreatic juice then is aspirated out of the duct as it is produced. The output of pancreatic bicarbonate, protease, amylase, and lipase are measured. This test is gaining popularity because most patients undergo ERCP at some point in their evaluation.
Indirect tests: Noninvasive tests of pancreatic function have been developed for detecting chronic pancreatitis. In principle, these tests work via oral administration of a complex substance that is hydrolyzed by a specific pancreatic enzyme to release a marker substance. The intestine absorbs the marker, which then is measured in the serum or urine. These tests are capable of detecting moderate-to-severe chronic pancreatitis. The presence of renal, intestinal, and liver disease may interfere with the accuracy of these tests. Neither currently is freely available in the United States.
http://www.emedicine.com/med/topic1721.htm

Gary Fry

2006-06-12T13:35:00.000+09:30

Gary and Rhonda Fry

Gary Fry August 12 1957 to April 30 2006

On April 30th 2006 Gary Fry passed away leaving behind his much loved wife Rhonda who’s battles with Chronic Pancreatitis was the inspiration for the creation of the Pancreatitis Message Board(PMB). Gary didn’t just create a great place where you posted a message, he created a family atmosphere and welcomed unreservedly anyone who wanted to post and make themselves known. The sense of family and community has always been a special feature of this board and through this Gary helped so many people who suffer pancreas related problems many of whom may never have actually made a post on the board but read often. He also kept it going through some very hard times but he had enough compassion/kindness in him to realize how much the many members of the community he had created depended on his board and he chose never to give up on it. Gary you are much loved and will be sorely missed,
I struggled to write about what Gary meant to the many people who frequent the PMB. So the best way I could think of was to take a selection of the many posts and e-mails that accompanied the sad news of Gary’s death.

From Alma

I first met Gary in the mid to late 90’s. I had been diagnosed with chronic pancreatitis in 1995 and was playing around on the computer learning how to navigate the internet. I found a site made by a person by the name of Bruce. His site was nothing but pancreas information and stories. I cried like a baby when I read the stories of others who had chronic pancreatitis. It was like finally someone could to relate and understand what I was going through. There was a link to other sites on Bruce’s site and I went through all of them. On one of the links I clicked on I immediately knew I had found a safe haven. I emailed Gary and we emailed each other back and forth and he had a message board he had started so his wife Rhonda could have someone to talk with that knew what she was going through. It was like we clicked immediately as friends. On the first message board there was not a lot of us and what there was instantly felt like family members that had known each other all their lives.
Gary showed me how to make a web site using a site on the internet that helps you do it. I still had questions and he would help me with them. I learned a lot from Gary not only about message boards and web pages but about life in general. His wife was very ill quite often but he never once complained to me about it. He always wanted to be there for her and was always there for her.
Another thing that brought Gary and myself together is a common love for Bluegrass Music. We both loved the bluegrass sound so we not only had pancreatitis in common but we were both country hicks and we loved this style of music. I even sent him a tape one time of a song I sang to get him to let me know how I was doing. He was honest and helpful. I never will be a true singer but he saw and understood that singing Southern Gospel which includes some bluegrass music, was for me a way to worship my God. Not many people understand that but Gary did from the beginning.
We contacted each other every day for some reason or another, be it me learning how to make web pages or dealing with the pain of cp or just a friendly chat to pass the time. We quickly became like brother and sister. We had our ups and downs like siblings also but we never ever gave up on each other. I will miss him terribly as I know his family will too. Family came first with him and he loved Rhonda with all his heart and more if it was possible. He was ever mindful that Mike could be sent to Iraq and worried about that a lot in the past couple of yrs.
Gary was always supportive of those that posted on the message boards he made. He did not put up with arguing and many times I myself would get in trouble for posting in an argumentative way. Being a very close friend did not stop him from scolding me either. Most times he scolded me in a private email and I really appreciated him for that. He was our rock of Gibraltar when we needed him to be and I don’t see how the board will function without him. I know it will never be the same with him gone. I never dreamed in a million years he would pass on before I did because I was the one with pancreas problems not him. It was a huge shock to find out he had died. Although I had not heard much from him lately I will miss him terribly. Just knowing he was there should I want to email him gave me a sense of security. That security is gone now and there will never be another Gary Fry for me nor will any of the message boards I see on the internet compare in any way to Gary’s board. In honor of him we are keeping the board he made up and running. It is different from other message boards on the internet in the fact that it is not censored. You can say what you want within reason and we all feel like one big family. The board has gotten larger each year and that is because Gary allowed it to be a family oriented board without having to have passwords and approval of a post, etc. I will always hold near to my heart the memories of Gary and his love for Rhonda and Bluegrass Music.

"THANK YOU GARY FOR YOUR CREATION OF THIS BOARD AND LOVE AND SUPPORT YOU HAVE GIVEN ALL OF US."

“It hasn't been easy I know, but you kept right on doing what you could to inform anyone who needed information about chronic pancreatitis. You will never be forgotten.”
Alma
aka: firstwin

Posted by Cindy on May 08, 2006
Taken from an e-mail from Gary to Cindy this was sent to me as is shown here:

“This group is the first to have a Pancreatitis specific message board on the internet. It is the longest running Pancreatitis specific message board as well. I started it in June of 1997 on a different server than it is now. We have moved several times due to different circumstances., usually the server shutting down.”

From Gary’s Sister DiAnn

“I have something that you may like to read about him. It will definitely give you and idea what kind of person he was . He worked in the coal mines and when there was an explosion he was there more than once to help and at times it got pretty gruesome.”
“In 1997 while he was going to college he was one of two people to receive a scholarship called the Felton Patton Memorial Scholarship”
The people on the Pancreatitis were an extended family to him and when we talked he often talked about the people on the board as if I should know them. I did get to the point that I felt like I knew some of them….”.

The excerpt on the right is from the paper clipping below

Subject: Re:Official Resignation as Administrtaor - CJ (c.j.) is new Administrater.
From: Gary
To: All
Date Posted: 21:12:15 12/14/05
Message:

“Wow ALma; I don't know where to start! It has been a two way street, we have been there for each other I think. We probably have been more like family, because we, as many do not know, have had our own ups and downs, (very few and nothing really serious), behind the scene and off the board. But like family, we have always healed our wounds and been able to forgive each other and go forward and leave the past behind. But most of all we were there for each other through the very tough times and we laughed a lot at the good times. I think we have even laughed at our self sometimes :)……”

Posted by Larry on May 02, 2006

I just received an email from Mike Fry who stated his father, Gary Fry, passed away this passed Sunday. If this is true, it is truly a very sad moment for all of us.
Can someone else verify this for us? There was an email address in the email that I received that I may respond back to.
I apologize if this seems so blunt, but I really did not know Gary was doing so bad.

Posted by Chuck on May 02, 2006

I just called the information line at Hampton Funeral Home in Barbourville. Gary Lee Fry did indeed die on Sunday. His funeral will be held Thursday at 1 PM.
I am so sorry to confirm the notice from his son. Gary was a very special person. He put his heart and soul into starting and running this board when Rhonda first was diagnosed. He has been a good friend and will be sorely missed.

Rest in Peace, Buddy.

Chuck

Posted by Brett on May 03, 2006

“Rhonda if you are reading this then please accept my condolences. Gary was a special person who has had a huge impact in my life by providing this special place. For that I am eternally grateful and forever in his debt. I can only imagine the pain you are in and hope that you will find peace for yourself.”

Rest in peace Gary, you will be missed

Posted by Pete on May 03, 2006

“I am truly saddened by Gary's untimely passing. He corresponded with me quite often when I joined this board in July'04.I will be forever grateful for him starting this board.Rhonda...if you read this, please accept my heartfelt sympathies for your loss. You will be in my prayers. I know Gary will be watching over us now from above. God has a special plan for him. I am truly going to miss him...a fine measure of a man!”

Pete(Fla.)

Posted by Christine on May 03, 2006

“i just want to offer my deepest condolences to Gary’s wife and family. i am so grateful to him for all his hard work with this board. it has been a life saver and he has made a difference in so many peoples lives that are suffering with this. i am so, so sorry. thank you Gary, rest in peace.“

Posted by Trisha on May 03, 2006

“What can i say that's not already been said. My thoughts and prayers go out to all his family and friends.I don't honestly know were i would be today if i never found this message board. Gary has helped everyone of us and that say's something about a person.
Rest in peace Gary......Thanks.”

Posted by Pam on May 03, 2006

“My sympathies as well. I saw that Gary last posted on 4/18...he seemed uplifted that this board was active. I hope that gave him joy and peace.”

Pam

Posted by Diane on May 03, 2006:

"REST IN PEACE... a special thank you for this board Gary... from those that post and those that come here as I do to, just read and learn. You and this board have given so much to those who suffer from this horrid disease. Deepest regrets to Rhonda and all that love you."

Diane

Posted by Christine Stanborough on May 03, 2006:

“RhondaTo say Gary was special is such an understatement. God bless you Rhonda your loss is immense and I just hope that our words give you some comfort. You and your family are in our thoughts and prayers.”

Kind regardsChristine

Posted by laurie on May 03, 2006:

“I just want to add my condolences to his family and friends. I am also shocked and profoundly saddened. I missed his posts but took it for granted that he was always going to be here to keep in touch with his legacy.
As far as the board goes with Carol....I think because it was his decision to dedicate this board to her memory that it should be respected. I think that it is a tribute to the person he was that he did this and to change it now would somehow not honour his wishes. Unless of course, there are other issues that his family wish to address. Just my thoughts, such as they are....”

laurie

Posted by Vickie on May 03, 2006:

.”Gary, we've had many conversations down the years and you've been a wonderful friend”

Vickie

Posted by judylu on May 03, 2006:

“I only hope he is at peace now. My heart goes out to Rhonda and the rest of his family and friends. He is surely missed and will be remembered well.”

Posted by Tami on May 04, 2006:

“I found this board in September of last year, and it has been my salvation with this disease. To find so many other people that can truly relate and sympathize as to what you are going through is not only priceless, but very much needed. Gary is and always will be a true hero to me, to stand so vigilantly by his wife’s side during her illness, to offer so much support and knowledge to others going through CP, what a true saint. Rhonda, I don't know you personally, but I am very sorry for what you are going through, your husband loved you so very much and you could just hear it in every word he had to say about you. You and your family are in my prayers, and I will pray for strength during this very difficult time.”

Tami McClurg

Posted by Lorie on May 03, 2006:

“I did not want to come on the board this morning, I waited 2 hours for fear of knowing that Gary has passed away. My heart hurts and goes out to Rhonda and all of Gary's family. Rhonda if you are reading the board please know that my heart goes out to you. I would like for you to know how much Gary has meant to me. Gary was my salvation in 1997 when I found the Pancreatitis message board. I felt alone and confused over my disease. I had so many questions, fears and needed desperately to know what all of this meant and if anyone else was feeling what I was feeling. My husband is supportive, but I don't know that anyone can imagine how we all feel unless you actually walk in our shoes.Gary brought all of us together as a family, none of us would even know each other if Gary had not brought us together with this board. For this we will always remember Gary and for me he will always hold a very special place in my heart. I can't even begin to say everything I am thinking right now. I am still so very shocked. Rhonda you more then anyone knows how much Gary loves you, he is one the most supportive husbands I know he always talked about you with so much love in his heart.Gary, and his passion for music brought joy to many lives. Gary, will be missed greatly. He had a way of sharing his passion's in life through the web. I know God has a plan for him and he is looking over all of us
Rest in peace Gary, Rest in peace.
My condolences to all of Gary's Family.”

Lorie Bledsoe

From CJ

I came across "Gary's board" in a desperate search to figure out what was wrong with my husband. I had pretty much figured it down to gallbladder or pancreas. After removing the gall bladder it went down hill, leaving pancreatic issues a guarantee. Gary's board, became my rock, while I sat up late nights searching and comparing info, I could always come back and post and ask questions and get valuable LIFE experiences from others who had already been there and done that. It helped to be able to discuss tests/treatments/symptoms so that I could choose the best path for ourselves. Over the years, posting our journey and reading and living thru others journeys, the hardships the laughter and the frustration, we have all become a large extended family. What I find wondrous is thru it all is that we continue to flourish! Chronic disease destroys one financially, emotionally, physically. It alienates you from your real families and friends and this board has been the replacement for both. Thankfully Gary, in his search for information and support could foresee a need for such a place!! Many times people come up with ideas and thoughts but do not put them into action. By Gary's ONE action of opening a "home" for people to rely on for support, and advice and personal perspectives and thoughts he began to create the biggest form of treatment we could receive. That treatment of Love, understanding and unconditional acceptance has been a beacon and drawn people from all over this world to stand in support of one another and we will continue to shine and light the way, helping others who are behind walk a path that is new to them, familiar to others and old to some. By helping one another we are helping ourselves and make the path a little less difficult for others to tread. Hopefully the path blazed by Gary will be worn smooth, and any newly found pancreatic sufferer and their families will have a very easy walk towards a cure and coping with the disease. Gary, Thanks for being there and being who you always were! Your life testimony of compassion and giving will not be forgotten but exalted thru our continuing works!

From Cindy

“Cant even express to Gary/Rhonda how much the creation of the board has meant to me. Like the rest of you know having this condition that those that don’t have it just can’t understand you 100% and what going thru. This place to come-the board has become over the years with some like extended family to me and to my son Brandon even if we live states/country away like we are so close. I have gained some good friends thru this board including Gary and if it wasn’t for him that would never be-we would have never been brought together for a life of friendship. And one day when Brandon is older and knows/understands my condition and friends over the years he will know about 'Uncle Gary' as well.

Gary you will be missed”

Cindy M

Posted by Cindy on May 08, 2006:

“I came on the board/around since 99. As a lot of you know being the first later on to get pregnant with CP and a lot of you went thru each step with me especially the ups and downs and when I was in the hospital 1 1/2 months while pregnant. For me I would like something said for Gary having to do with that and what he wrote to me when he resigned from board to only be a user of it because some of you called yourselves/I called you 'aunt/nana' and him Uncle Gary he said to Brandon which shows the closeness, caring etc. He called me in the hospital too and helped me with some ?s and worries I had, always included him on emails w/pictures of brandon growing up now 2 1/2 + and he always wrote back such nice things but this one I found hits home and even the part for us to be there/help CJ he knew and went thru some rough times with the board and stuck it out/did what he had to do and best for the board up till when he felt he had to resign. Gary/Uncle Gary -you will be missed tremendously”

Cindy and Brandon

Posted by Gary on December 17, 2005 at 13:02:49:

Cindy;“You, I will never forget. You will always be our first member to deliver a baby, little Brandon, in our group of Pancreatitis sufferer's here. You have always and will always be a friend. Say hello to Brian and little Brandon. Keep in touch. And most of all, lets all help C.J., it is a pretty rough job at times”.

Gary

Finally this was posted by Joan and I thought it was a great way to finish

Posted by Joan on May 12, 2006

I ran across this poem today and when I read it made me think of Gary so I thought I would share it with you guys....

THE BROKEN CHAIN

We little knew that morning that God was going to call your name.
In life we loved you dearly; in death we do the same.
It broke our hearts to lose you, you did not go alone;
for part of us went with you, the day God called you home.
You left us peaceful memories, your love is still our guide;
and though we cannot see you, you are always at our side.
Our family chain is broken, and nothing seems the same;
but as God calls us one by one, the chain will link again.

Author Unknown

Medical Malpractice

2006-06-11T10:12:00.000+09:30

Each year, over 100,000 people are killed by preventable medical errors, due to negligence or wrongdoing. Many more are seriously or permanently injured, disfigured or disabled.The leadership in the House of Representatives is promoting legislation, written by the insurance industry and HMOs, which would restrict the ability of Americans injured by medical malpractice to hold accountable those who caused them harm.

The legislation would create a "one size fits all" system for people injured in a medical setting or nursing home. The limits would apply no matter how severe the harm - even if the wrong limb was amputated, an unnecessary mastectomy was performed, or even in cases involving the death of a child. Congress has their priorities mixed up. Shouldn't we be talking about protecting the health and safety of patients, rather than protecting Congress' corporate friends in the health care, insurance and HMO industries.Urge Congress to oppose any legislation seeking to restrict the rights of people through so-called medical malpractice "reform."

http://www.thepetitionsite.com/takeaction
/991264371?z00m=88688&z00m=88688&ltl=1149961706

The truth about Headaches

2006-05-31T09:18:00.000+09:30

Dr. David Buchholz: The Truth about Headaches
By The 700 Club

CBN.com – If you're like most people, you're probably confused about the whole subject of headaches. You may wonder, Do I have migraine? Or do I have a brain tumor? Could it be an aneurysm? What about my tension headaches? Or sinus headaches? Is it arthritis in my neck, or a pinched nerve, or am I just stressed out, or is it my hormones, or what is it? You're not the only one confused and frustrated about headaches.
All headaches arise from a single mechanism - the mechanism of migraine - which generates painful blood vessel swelling when activated by specific triggers. This headache-generating mechanism, which produces not only headaches but also other symptoms including dizziness, neck stiffness, sinus congestion and many more, can be controlled. Control starts with reducing your exposure to some of the triggers, especially certain food and medications. If trigger avoidance alone isn't effective, preventive medication, which blocks the mechanism, can be added. Painkillers, on the other hand, lead you to lose control. Many headache sufferers spin farther and farther out of control in a vicious cycle of victimization by headaches and dependence on painkillers.
DIETARY TRIGGERSDr. Buchholz says there are many unavoidable or difficult to avoid migraine triggers such as barometric pressure and weather changes, hormonal fluctuations, sensory stimuli, physical exertion, sleep deprivation, and stress. With these triggers there is little you can do to avoid these situations. There are however avoidable triggers in which you can begin to take control of your headaches. Avoidable triggers are for the most part, things that are swallowed: certain foods and beverages, and medications. Some potential dietary triggers are listed below. Dr. Buchholz cautions that everyone is different, and it may be that not every one of the foods and beverages that most commonly cause headaches is a trigger for you.
Avoidable dietary triggers.

Caffeine - Coffee, tea, iced tea and cola. Even decaf coffee and tea may be a problem. Try caffeine-free tea without citrus and other trigger flavors.

Chocolate - White chocolate (no cocoa) is okay; carob is questionable.

Processed meats and fish - Aged, canned, cured, fermented, marinated, smoked, tenderized - or preserved with nitrites or nitrates.

Cheese and other dairy products - The more aged, the worse. Permissible cheeses include cottage cheese, ricotta, cream cheese and good-quality American cheese.

Nuts - Avoid all kinds, as well as nut butters. Seeds are okay.

Vinegar - Clear or distilled vinegar is allowable. Don't overdo condiments made with vinegar such as mustard.

Certain fruits and juices - Citrus fruits and their juices as well as bananas and dried fruit preserved with sulfites.

Certain vegetables - Avoid onions, sauerkraut, pea pods and certain beans.

Aspartame - Nutrasweet and saccharin. Sucralose (Splenda) isn't a problem.

Fresh yeast-risen baked goods - Less than one day old: homemade or restaurant baked breads such as sourdough.

It's likely that you can eventually tolerate some of the dietary triggers in limited quantities. Before reintroducing these items into your diet, make sure you have achieved headache control and maintained it for four months or more. If you add back an item and headaches recur then stay away from it. If you add back an item and maintain headache control then keep this item as part of your diet. Another benefit in following the migraine prevention diet is that you will not only have fewer headaches, but also shed unwanted pounds. For effective weight loss, Dr. Buchholz says you should concentrate on eating food that is fresh and healthy and avoid foods that are processed. Foods that are processed may contain chemical triggers such as MSG, which can cause headaches.
PREVENTION OF HEADACHESBeyond dietary modification, you can make other lifestyle choices to help control your headaches. Regularity is key: you should sleep, eat and exercise on a regular basis. Get enough sleep each night, seven to eight hours or more, and don't oversleep sporadically, as on weekends.Skipping meals is a common trigger for migraine. Stay on schedule for three meals a day, no more than six to eight hours apart. Snack in between if you wish, but only on nonrestricted items. Exercise helps both body and mind, and in both ways helps to control headaches. Regular exercise is a means of relieving stress and thereby helps in reducing your trigger load. Exercise also enhances your migraine threshold by stimulating endorphins in your brain and helping to block the mechanism that causes headaches.

Enzymes

2006-05-26T20:47:00.000+09:30

Posted by Cindy on May 26, 2006

Digestion begins in the mouth where we physically break down foods with our tongue and teeth. The food particles then travel to the stomach where they are further digested by the acidic stomach juices.As food leaves the stomach and enters the small intestine, several digestive fluids are added. These fluids contain enzymes, which aid in the digestive process.For example, the pancreas secretes three enzymes into the small intestine: amylase, protease, and lipase. These enzymes are also produced by the intestinal wall. We also get important enzymes from the foods we eat. However modern cooking practices and food processing kills many of these enzymes before we ingest them. This lowers the amount of enzymes in our digestive system and slows the digestive process.Many people take supplements that contain plant enzymes that catalyze, or stimulate, the digestion process. These supplements often contain amylase, protease and lipase - enzymes that help take some of the work away from organs like the pancreas, which may be under undue stress due to modern eating habits.Each of these enzymes have special binding spots called receptors that help it match with and bind to a particular type of nutrient.For example amylase digests carbohydrates such as the starches found in potatoes and pasta. Proteases help the body break down protein found in foods such as meat into tiny building blocks that can then be used to build and maintain the body's tissues. And lipases help the body break down fats and oils, which may help lower the amount of fats circulating in your blood stream.http://digestive.healthcentersonline.com/liverpancreasbiliary/then under Animations click on Enzymes.

Dangers of Too Much Acetaminophen!

2006-05-11T20:08:00.000+09:30

Dangers of Too Much Acetaminophen!

Acetaminophen (APAP) is the most widely used analgesic (pain killer). It is available in various formulations including: liquid, tablet, capsule, and suppository. APAP has an excellent safety profile when ingested appropriately, but liver toxicity can develop in acute overdoses or chronic ingestions.

Over-the-counter combination products can be have hidden dangers especially if multiple medications containing acetaminophen are taken together. Unfortunately, initial signs and symptoms of acetaminophen toxicity are non-specific (nausea and vomiting) or absent. To avoid liver damage from acetaminophen, do not take more than 1 gram (1,000mg) of acetaminophen at once, do not exceed 4 grams of acetaminophen in 24 hours, and always check to see if over-the-counter or prescription medications contain acetaminophen. For children, do not exceed 10-15mg/kg/dose of acetaminophen and do not exceed five doses or 2.6 grams in 24 hours. If you are unsure about any medication containing acetaminophen, contact the poison center at 1-800-222-1222.

Scenarios which often result in inadvertent acetaminophen overdose include:

Children being given Tylenol Children’s to relieve a fever over several days

Treating pain (headache, toothache, backache etc.) with various prescriptions and over-the-counter pain medications

Treating a cold, allergies, and stuffed-up nose at the same time

Ingesting various generic non-aspirin products

Reasons for unintentional overdoses appear to be multi-factorial and include:

Simultaneous use of multiple products containing APAP

Inadvertently exceeding the maximum daily dose of 4 grams (4,000mg) of APAP in adults or 2.6 grams (2,600mg) of APAP in children

Unaware of various over-the-counter (OTC) products that contain APAP

Co-ingesting OTC’s and prescription medications that contain APAP

Common prescription medications containing Acetaminophen include:

Acetaminophen and Hydrocodone (Vicodin, Lortab)

Acetaminophen and Propoxyphene (Darvocet)

Acetaminophen and Oxycodone (Percocet, Endocet, Roxicet)

Acetaminophen and Tramadol (Ultracet)

Acetaminophen and Butalbital and Caffeine (Fioricet)

Acetaminophen and Isometheptene and Dichloralphenazone (Midrin)

Common over-the-counter preparations containing Acetaminophen:

Acetaminophen
 Tylenol, Non Aspirin Pain Relief, Tylenol Children’s, Tylenol Infants, Tylenol Sore Throat

Acetaminophen and Diphenhydramine
 Excedrin PM, Tylenol PM, Legatrin PM, Sominex Pain, Tylenol Severe Allergy, Anacin PM Aspirin Free

Acetaminophen and Pseudoephedrine
 Alka Seltzer Plus Cold and Sinus, Children’s Tylenol Sinus, Infant’s Tylenol Cold, Sinutab Sinus Maximum Strength Without Drowsiness, Sudafed Cold and Sinus, Sudafed Sinus Headache

Acetaminophen and Aspirin and Caffeine
 Excedrin, Genaced, Goody’s Extra Strength Headache Powder, Vanquish Extra Strength Pain Reliever

Acetaminophen and Pseudoephedrine and Chlorpheniramine
 Alka Seltzer Plus Cold, Children’s Tylenol Cold, Comtrex Allergy Sinus, Thera-Flu Flu and Cold, Sinutab Sinus Allergy

These are just some of the many preparations containing acetaminophen on the market.
This is taken from Minnesota Poison Control Center web site

Top Ten Reasons to Fire your Doctor

2006-04-12T09:56:00.000+09:30

Posted by cj on April 11, 2006 at 14:58:28:
Top 10 Reasons To Fire Your DoctorGuide Picks
Doctors have strengths and weaknesses. How does your doctor's "bedside manner" match up with your personality?
Are you confident in your doctor's ability? Do you feel that you understand the directives and decisions made by your doctor? Are you encouraged to ask questions? Is the overall experience at your doctor's office positive?
The relationship between a doctor and patient is very important. If you're answering no to most of the questions it may be time for a change.
1) Lack Of Confidence In Doctor's AbilityA patient must trust their doctor. Patients are more likely to be compliant with their treatment plan if they have confidence in their doctor's ability. A patient consults with a doctor for their expertise as a diagnostician and ability to problem-solve. A patient should not routinely leave the doctor's office feeling uneasy about decisions and recommendations which are made by the doctor. If you find yourself doing that, it may be time to fire your doctor.
2) Lack Of Continuity Between VisitsThe nature of chronic illness implies you will be seeing a doctor many times to help you manage your condition. With copious notes in your medical chart, your doctor should be able to recall your prior visit and gauge your progress. Doctors are busy and they see many patients, so it's not always perfect. If you constantly have to repeat yourself and if you feel that your doctor isn't following along, it may be time to fire your doctor.
3) Questions Are Not WelcomePatients go to doctors in search of answers. Patients want answers to:
what's wrong with me? how are we going to treat the condition? what can I expect? what are my options?
Some doctors allow a reasonable amount of time for patient questions. Other doctors are unapproachable and discourage questions. If it's difficult to have a dialogue with your doctor about your health care, it may be time to fire your doctor.
4) Doctor Is Not Forthcoming Does your doctor share all pertinent diagnostic test results with you? Does your doctor share why a specific test is being ordered or why a specific treatment plan has been chosen over another? For example:
Your doctor may give you an order for an MRI. Your doctor may tell you why you need to have an MRI and explain what he is trying to rule out, and then give you the order for the MRI.
If you feel uninformed more often than not, it may be time to fire your doctor.
5) Doctor Is Cold And UnsympatheticIt's important that you understand your doctor, but it is equally important that you be understood by your doctor. Does your doctor understand how your medical condition impacts various aspects of your life? Is your doctor sympathetic about your problem or is your doctor's demeanor cold and abrupt? You must feel that your doctor truly cares about your well-being, otherwise it may be time to fire your doctor.
6) Excessively Long Wait To Get An AppointmentYou may encounter a long waiting period when you try to set up a doctor appointment. Doctors have very busy schedules, especially specialists and surgeons. As the joke goes - I wouldn't want to go to a doctor who will see you the next day. A busy doctor is often a popular doctor with a great reputation. However, by waiting too long for an appointment, you may be compromising your health. If the wait seems unreasonable, find another doctor.
7) Doctor Is Always Rushed Do you have your doctor's full attention during your appointments, or do you sense that your doctor's mind is cluttered by other matters unrelated to you? Do you feel that you're being hurried? Has your doctor ever backed out of the room before you were able to ask all of your questions? If you are left feeling that not enough time is devoted to you during your appointments, it may be time to fire your doctor.
8) Inconvenient LocationIt can be stressful and inconvenient to have to drive a long distance to see your doctor, especially if you have mobility problems. Some patients who live in rural areas have fewer options, but convenience is a factor to be considered. Where will the doctor send you for blood tests, x-rays, and other tests? What are your doctor's hospital affiliations? Be sure your situation is either convenient or agreeable to you, otherwise you may want to find another doctor.
9) Cost / CoverageIf your insurance does not cover your doctor's fees, it is unlikely you would want to stay with that doctor. Know the details of your individual health plan and be certain that your doctor is available to you on the provider list. If not, you may want to find another doctor so your medical costs will be covered by your insurance.
10) Doctor Is Not RespectfulIs your doctor harsh when speaking to you? Does your doctor consider your fears and apprehension when making decisions, or are your feelings disregarded? Does your doctor respect that your time is as important as their own, or does your doctor leave you languishing in the waiting room for unreasonably long periods of time? Do you feel respected as a person by your doctor? If not, it may be time to fire your doctor.
Related ResourcesHow Would You Rate Your Doctor? Should You Change Your Doctor? How To Choose The Right Doctor Last update 4/1/06

2006-04-02T22:28:00.000+09:30

PAIN MYTHS

Myth #1: "It's only subjective." Pain is a subjective construct and each individual learns the meaning of pain through early life experiences (Merskey & Bogduk, 1994). In science, an objective phenomenon is one that is "perceptible to the external senses," (Dorland's, 1994, p. 1166) while a subjective phenomenon is one that pertains to or is "perceived only by the affected individual; not perceptible to the senses of another person" (Dorland's, 1994, p. 1595). Behavioral observations and patient self-report indirectly measure subjective phenomena; direct methods, e.g., laboratory tests or radiology films, can measure objective phenomena. Physicians treat about 70% of all patients for subjective complaints (Harsha, 1990), so chronic pain patients are hardly unusual. What makes chronic pain patients unique is that they generally do not get better spontaneously. Indeed, they often do not get better after considerable intervention, especially after incorrect treatment strategies...................

For the full article follow this site......Countering Chronic Pain Myths

Enzymes

2006-03-17T20:19:00.000+10:30

Plant Enzymes & Probiotics Active Ingredients(Each 1/4 tsp. or gram)
Alpha & Beta Amylase –3,150 DUProteases – 20,500 HUTLipase – 265 LUCellulase – 110 CUHemicellulase – 100 HCUBromelain – 20,000 FCCProbiotic (Bacillus coagulans) – 600 Million CFU
Nutritional InformationCrude Protein- 5.0% min.,Crude Fat- 0%,Crude Fiber- 0%,Moisture- 6.0% max.
Contains no lactose, sugars or preservatives. Add 1/4 teaspoon to each cup of food Plant enzymes: $10.75
Digestive enzymes are special types of protein molecules that catalyzethe breakdown of food into components that can be utilized by the body.These proteins are not stored in the body but are released based on theanticipation aroma or actual presence of food in the digestive system.Because they are not stored they must be taken with each meal,preferably with the food. Merritt's enzymes contain a blend of plant andmicrobial produced enzymes. None of them are from animal sources.
Each enzyme is highly specific as to the class of food it works on andthe temperature and pH of its effective range of activity. Animalderived enzymes will work in only one area of the digestive system,while plant and microbial enzymes work throughout the whole system, frommouth through the stomach into the intestines. As the body ages lessenzymes are produced and supplementation is necessary to assure optimumhealth.
To maintain optimum health in an animal it needs to be fed an optimum,diet, but also needs to have digestive efficiency necessary toassimilate the food ingredients. The digestive efficiency can be reducedby stress of any sort, excitement , anxiety (travel separation, workingstress and so on. To insure optimum digestion and health we recommendthe addition of this supplement to each meal. For optimum utilizationthe supplement should be added to the food and should be moistenedshortly before feeding to be effective.
Since Merritt's enzymes are derived from plant and microbial sourcesthey are active throughout the whole gastrointestinal tract not in aspecific section, as animal derived enzymes are. These enzymes areactive from pH of 3 to 9 and at a temperature of about 100 o F. Animalderived enzymes either work in the stomach at a low pH or in theintestine at much higher pH. Since ours work over a broader range theyare active longer in the system at reducing the food into usable components.
Back to TopEnzymes; All Natural Plant Base Enzymes by Cell Tech [new window][frame][cache][preview][close preview][clusters]... CTI Enzymes contain a combination of enzymes to help break down all types of ... E-12 Super Enzymes - a superior blend of plant-based enzymes plus Cell Tech Super ...websites.celltech.com/sbgalgae01/files/enzymes.htm-Ask 1, Ask 7, MSN 17Enzyme Health [new window][frame][cache][preview][close preview][clusters]are those enzymes that are present only in raw food and contain varying quantities of the four basic types of plant enzymes: protease used in protein digestion, amylase for carbohydrate digestion, ...www.hum.org/enzyme_health.html-Wisenut 6, Ask 34, MSN 82Enzymes - plant enzymes, or food enzymes? Enzymes move our muscles ... [new window][frame][cache][preview][close preview][clusters]Plants are dependent on free enzymes in the soil to help make plant food, and suffer ... the integrity of metabolic enzymes, and abuse the enzymes' potential, we are inviting the most serious types ...www.simplecom.net/timeless/digest.htm-MSN 9, Ask 16

Addiction Vs Dependance

2006-03-01T10:31:00.000+10:30

Pain pills: Avoiding addiction

There's little risk of becoming addicted to prescription pain medications if you follow your doctor's directions for use.

The injury was months ago and you've done everything your doctor suggested — stretching, strengthening exercises, ice, heat — but you still hurt.
Over-the-counter pain remedies aren't helping, and you'd like to try something stronger. But you're also somewhat hesitant. What about all the celebrities who've wound up addicted to prescription pain medication? Would that happen to you?
The short answer: Probably not.

What is addiction?
Pain specialists define addiction very precisely. The key component is that an addict uses a drug compulsively, despite the fact that it causes harm. A prime example is cigarettes. Most smokers know that cigarettes damage their health. Many want to quit, but can't overcome the craving. That's addiction.
People who are, or have been, addicted to one drug are at higher risk of becoming addicted to other drugs. Addictive disorders also tend to be inherited. If you have family members who abuse drugs or alcohol, you're at higher risk of the same problem.

Addiction vs. dependence
Some people confuse addiction with physical dependence, a condition that results in withdrawal symptoms if the drug is suddenly stopped.
Many types of nonaddictive drugs — including corticosteroids and beta blockers — can cause physical dependence. These types of drugs should not be stopped abruptly. Instead, the dosage should be reduced gradually, so the person can be weaned off the medication.
Addiction and physical dependence often occur together. But you can have addiction without physical dependence, and physical dependence without addiction.

Addictive pain medications
Some of the most addictive pain medications are opioids, a family of drugs that have effects similar to those of opium or morphine.
Commonly prescribed opioids include codeine, propoxyphene (Darvon, others), meperidine (Demerol, others), hydrocodone (Vicodin, others), hydromorphone (Dilaudid, others), oxycodone (OxyContin, others) and morphine (MS Contin, others).

Who's at risk?
The vast majority of people who take their pain medication as directed never become addicted, even during long-term use. The key is to take the medication exactly as prescribed by a physician. Frequent assessment and follow-up with your doctor will ensure that you're taking the safest and most effective amount of medication.
The addiction risk is higher for people who have a family or personal history of drug or alcohol abuse. This additional risk is lessened in people participating in 12-step recovery programs such as Alcoholics Anonymous and who have family support.

Mistaken identity
People with unrelieved chronic pain sometimes act in ways that appear to be addictive. They may be preoccupied with maintaining their supply of medicine or anxiously watch the clock so that they won't miss their next dose. These behaviors, called pseudoaddiction, typically stop once the person gets satisfactory pain relief.
It also is common for people to develop a tolerance to their pain medication, needing higher doses to achieve the same level of pain relief. This is normal, and not a sign of addiction. In some cases, tolerance proves to be helpful, as many of a drug's side effects may disappear once your body becomes more used to the medicine.

Be honest with your doctor
Tell your doctor if you have had a particular side effect from a pain medication in the past. Also share your personal and family history of substance abuse or addiction. Your doctor needs this information to choose the type of pain medication that will work best for you.

***********************************************************************

Taken from the Mayo clinic website

http://www.mayoclinic.com/health/pain-pill-addiction/PN00056

***********************************************************************

Nausea Help

2006-02-22T09:27:00.000+10:30

This will be an ongoing post to which I will add more information as it comes to hand. If there is something you wish to add please use “comments” and I will add it to the body of the post. These idea’s are not intended to replace any nausea treatment you are now receiving. These idea’s were posted on the PMB.

Robin H
“Zofran, 4 mg. by IV, is by far the best for me for nausea”
“classic (not diet!) Coca-Cola, at room temperature (cold will induce vomiting) and take a teaspoon at a time “
saltine crackers

CJ
mint tea
ginger tea
ginger ale soda7 up
crackersphenerganZofranKytrilCompazine,
Raglan
Inap
Levisin sublingual

Rhonda
Compazine

Jennifer
Phenergan
Zofran

Cindy
Reglan

Brett
Maxalon
Mint tea
Boiled candy
Ginger ale (ginger Soda) Must have real ginger in it
Ice cube held between joint of thumb and index finger

Pete
Saltine crackers(no salt)
Ginger Ale
Phenergran 25mg
flat Coke-room temp

Links From CJ

2006-01-30T22:44:00.000+10:30

Links From CJ:

New Additions 16-mar

http://www.enzymestuff.com/digestion.htm

_____________________________
Dr's Guide

Medical Alert Bracelet

HGI Home

InteliHealth

Medlounge

MiniMeta Searches

MED-HELP.COM

Medical Herbalism Online

Medical Matrix

Medical World Search

Medicine Net.Com

National Institute Of General Medicine

Team Surgery

Nutrition Reporter

US National Library of Medicine

University of Bristol Web

MD Virtual Library

Med Explorer

ACUTE PANCREATITIS

2006-01-30T12:20:00.000+10:30

ACUTE PANCREATITIS:
Symptoms:
Abdominal pain: Diffuse throughout the entire upper abdomen. May be localized in the midepigastrum and LUQ or RUQ. Radiation to the back. Pain reaches maximum intensity within 10-20 min and may appear like a perforated ulcer. Pain is moderate to severe. Can be unbearable and refractory to PO narcotics. Steady and boring. Little fluctuation in pain. No relief by change of position of bed.
Nausea and vomiting: Frequent. May be severe and last several hours. May turn into dry heaves. Vomiting does not relieve the intensity of the pain. Even with gallstone pancreatitis, there is no temporal relationship between eating and the onset of pain.
Physical Exam:
Vitals: HR may be ( to 100 to 150. BP may start high and then go lower as there is third spacing. Temp: may be normal and then rise to 101 to 103.
Respiration: May be shallow if there inflammatory exudate on the diaphragm. Limited diaphragmatic excursion if abd causes splinting of the abdomen. Dullness to percussion due to pleural effusion.
Abdomen: Tenderness in upper abdomen. Guarding, percussion tenderness. Distention of abdomen. Rarely rigid. Grey Turner sign: ecchymoses in one or both flanks. Cullen sign: ecchymoses of the periumbilical region due to pancreatic exudate
Lab diagnosis:
Amylase: Reflects leakage of pancreatic isoamylase into the systemic circulation. ( 75% of acute pancreatitis. Remains ( for 5 to 10 days. Usually 3x Nl. Limitations: Amylase not ( in all cases of pancreatitis.
Lack of specificity: Acute pancreatitis, pancreatic carcinoma, acute cholecystitis, common bile duct obstruction, perforation of viscous, intestinal ischemia, intestinal obstruction ,acute appendicitis, renal insufficiency, and many more.
Lipase: ( in pancreatitis to 3x normal. Normal is 20-250. More specific. Almost all lipase originates from the pancreas.
Limitations:
( Renal insufficiency: Lipase ( only when creatinine clearance is < 20 ml/min. Lipase level is usually 2x normal.
( Acute intra-abdominal conditions: Usually less than 3x normal.
Standard blood tests:
( ( WBC, serum glucose, AST, ALT, Alk phos, and serum bilirubin.
( Biliary vs. alcoholic pancreatitis: ALT > 150 96% specific for gallstone pancreatitis. However, sensitivity was only 48%. Therefore a level of < 150 does not exclude gallstone pancreatitis
Radiologic features:
Survey film: Anterior displacement of the stomach. Ileus of one or more loops of jejunum (called the sentinel loop), or any of the small intestine. Colon cutoff sign: Inflammation from head of pancreas that spreads to the proximal transverse colon that leads to spasm of this area and dilatation of the ascending colon. Possible calcified gallstones.
Chest radiography: limited diaphragmatic excursion, pulmonary infiltrates, or pleural effusion.
Barium Studies: Replaced by CT
Ultrasound: Presence of gallstone. Dilated CBD. Enlargement of pancreas
CT: Most common technique for evaluation of acute pancreatitis. The indications are:
( If mesenteric infarction or perforated ulcer cannot be excluded.
( Staging pancreatitis
( Defining the complications.
MRI: Same information as CT. Not currently used.
Differential Diagnosis:
Biliary Colic
Perforated hollow viscus
Mesenteric ischemia
Closed loop intestinal obstruction
Inferior wall MI
Dissecting aneurysm
Ectopic pregnancy
Predisposing conditions:
Gallstones: Responsible for 30 to 75% of all cases of acute pancreatitis. Caused by lodging of gallstone in the ampulla of vater. Pathogenesis remains undetermined. Thought to be obstruction of pancreatic outflow rather than regurgitation of bile into the pancreas. Others cases are caused by stones too small to image.
Alcohol: 30% of cases. Mechanism is unclear.
Hyperlipidemia: 4% of cases. Most occur in pts with uncontrolled DM and a Hx of hypertriglyceridemia. Typically pts will need levels greater than 1000. Levels between 500 and 1000 may occasionally cause pancreatitis.
Hereditary pancreatitis: Autosomal dominant with variable penetrance. Need identification of at least two family members. Episodes begin in childhood.
Hyperparathyroidism and Hypercalcemia: 0.5% of cases. Mechanism unclear.
Structural abnormalities:
Medications:
( Immunosuppressive agents
( Sulfonamides
( Abx: Metronidazole, tetracycline, and nitrofurantoin
( Valproic acid
( Corticosteroids
( Furosemide
( Estrogens
( Aldomet
( Pentamidine
( Octreotide
( Didanosine
Infectious agents:
( Viral: Coxsackie B, EBV, CMV, varicella, and Hep A, Hep B, Hep C.
( Bacterial: Tb, leptospirosis, brucellosis.
( Candida albicans
( Parasitic: C. Sinensis and ascaris.
Other: Vascular dz, ERCP, post-operative, pancreatic trauma, cystic fibrosis, pregnancy, and miscellaneous.
Classification by Ranson criteria:
These are signs that have prognostic significance. The criteria on admission are measures of the intensity of local inflammation. The other 6 reflect the development of systemic complications and the harmful effects of third spacing fluid. The higher the number of Ranson criteria a pt has the more severe the pancreatitis. A large study showed that a ranson score of 1.6 correlated with mild pancreatitis, 2.4 with severe pancreatitis, and 5.6 with lethal pancreatitis.
On admission:
Age > 55
WBC > 16,000
Glucose > 200
AST >250
LDH > 350

During first 48 hrs
1) Hct ( of > 10: a measure of hemoconcentration
2) BUN ( of >5: reflects renal failure
3) Ca <8: loss of nonionized calcium associated w/loss of serum albumin, fat saponification, and complex cascade ( calciuria.
4) Pa O2 < 60: respiratory failure
5) Base deficit > 4: metabolic acidosis and shock
6) Fluid sequestration > 6 L: difference between amount of fluids administered IV vs. losses from urine and NGT.

These criteria are good only for the first 48 hrs. These criteria are most useful to exclude severe disease. The overall sensitivity for the criteria is 57 to 85%, specificity is 68 to 85%, the positive predictive value is 50% and negative predictive value of 90%.
Medical Management:
Fluid Resuscitation: Large amounts of fluid are lost secondary to exudation of blood and plasma protein into the retro peritoneal space. There is also ( the formation and release of kinin peptides ( vasodilatation and ( vascular permeability. Fluid resuscitation prevents hypotension and renal insufficiency. Requirements may be in excess of 6 L per day and can exceed 10L to maintain adequate vol. Swan-Ganz may be helpful in determining adequacy of fluid resuscitation. Colloid should be used if albumin is < 2 g/l. If Hct ( to 25 then PRBC should be used to maintain Hct at 30.
Respiratory care: Major problems are atelectasis, pneumonia, pleural effusions, CHF and fatigue. ARDS may also develop. O2 should be measured constantly and given if needed. ARDS occurs on 2nd to 7th day of illness.
Cardiovascular care: ( in cardiac index and ( in peripheral vascular resistance. IV use of dopamine can help maintain systemic blood pressure.
Relief of pain: PCA MSO4 is preferred over Meperidine.
Nutritional support: TPN for 3 to 6 weeks. Switch to oral feedings if abdominal pain and tenderness have lessened, organ dysfunction improved, and pt is hungry. Start with small feedings.
Local Complications
1. Pancreatic inflammatory mass (phlegmon).
2. Pancreatic infection of necrotic tissue
3. Pancreatic abscess (bacterial infection)
4. Pancreatic pseudocyst (collection of fluid and debris which, in contrast to true cysts, do not have epithelial lining)
5. Pancreatic ascites (leak of pancreatic duct)
6. Involvement of adjacent organs by necrotizing pancreatitis
Systemic Complications
1) Pulmonary: Hypoxia and ARDS can occur due to ( surfactant due to circulating phospholipases, alveolar capillary leak.
2) Cardiovascular: ( intravascular vol or shock may occur due to "third spacing" of fluid into edematous retroperitoneal space. Kallikrein activation and bradykinin production can cause ( capillary permeability, vasodilation, and hypotension.
3) Hematologic: Circulating trypsin activates thrombin and plasmin with resulting DIC. ( Hct may occur due to retroperitoneal bleeding.
4) Gastrointestinal: GI bleeding may occur due to pancreatic inflammation affected the stomach, duodenum, or peri-pancreatic blood vessels, or due to gastric varices resultant from splenic vein thrombosis. Nausea and vomiting may occur due to ileus of small bowel adjacent to pancreatic inflammation.
5) Renal: Impaired kidney function due to hypoperfusion of the kidneys from ( intravascular volume.
6) Metabolic: Hypocalcemia may occur due to precipitation of Ca in fatty soaps in the retroperitoneum (saponification of Ca by fatty acids in areas of fat necrosis), ( serum albumin, and/or ( PTH secretion.
7) CNS (psychosis)
8) Fat necrosis. Occurs in pancreas and in other sites, such as subcutaneous tissue. Related to release of lipase and phospholipase.
9) Endocrine. Hyperglycemia may occur if insulin production is impaired. Need to have 90% destroyed before get problem.
10) Fevers. Related to pancreatic inflammation and cytokine release.
11) Ascites: fluid leaking from pancreas. ( amylase and lipase.
12) Pseudocyts: Not true cysts. Still dealing with residual and fluid collection. About 6 weeks. Some will resolve on their own. Some need more active treatment.
CHRONIC PANCREATITIS
Chronic inflammatory process of the pancreas which generally manifests as pain and/or malabsorption. It can cause exocrine and endocrine insufficiency, especially when >90% of pancreatic function impaired.
Etiology
*****Alcohol >80%****
Idiopathic
Cystic Fibrosis: cause of occult pancreatitis.
Hereditary
Protein malnutrition
Pathophysiology
Uncertain. Associated with ( precipitation of protein (inspissated enzymes) w/in ducts ( duct obstruction, dilation, fibrosis, and calcification. Induced stone formation w/in ducts in pancreas.
Recurrent pancreatitis ( Chronic pancreatic changes.
Alcohol toxic to pancreas. Disrupts normal defenses against autodigestion.
Abnormal trypsin resistance to trypsin degradation.
Clinical Features
1) Epigastric pain: constant or intermittent. Etiology of pain unclear, but may be related to pancreatic duct/tissue HTN (actual stretching) or to peri-pancreatic nerve damage.
2) Steatorrhea occurs when >90% of gland ceases to function. If from pancreatic. Do they see oil drops in stool. Has to be pancreatic insufficiency. Maldigestion.
3) DM:
4) Protein maldigestion is less common than fat maldigestion.
5) Malabsorption of fat soluble vitamins (ADEK) and vitamin B12 may occur. Vitamin B12 deficiency occurs because B12 binds to non-intrinsic factor proteins which must be cleaved by pancreatic enzymes to allow binding to intrinsic factor for absorption.
Diagnostic Evaluation
Unfortunately no clinical "gold standard" exists. Pancreatic biopsy is generally not performed for fear of inducing acute pancreatitis. Severe cases are easy to diagnose with pancreatic calcifications on xray, steatorrhea, and diabetes mellitus.
Anatomic Imaging Studies
( Abd radiograph ( calcification in severe cases.
( Ultrasound (trans-abdominal or endoscopic) - shows calcification, thickening pancreatic duct wall, dilated and irregular pancreatic duct, and lobular appearance
( CT scan - shows calcifications and a dilated pancreatic duct
( ERCP - shows dilated and irregular pancreatic duct with strictures, possible stones, and dilated side branches.
Functional Studies
1. Qualitative and quantitative fecal fat: > 7 gm in 24 hrs will confim diagnosis.
2. Secretin stimulation test.: release of pancreatic enzymes and release of bicarb.
3. Bentiromide test.
Management
1. *****Avoid alcohol *****
2. Long-term narcotic pain medication is often required.
3. Tricyclic antidepressants can help raise sensory pain threshold.
4. Surgical or endoscopic treatment may help if there is a focal pancreatic duct stricture.
5. Oral ingestion of pancreatic enzymes results in negative feedback to the pancreas, decreases enzyme secretion, improves steatorrhea, and may improve pain in mild-moderate severity cases.
6 Octreotide may have a role in selected cases.
HEREDITARY PANCREATITIS
Autosomal dominant disease with 80% penetrance.
Symptoms: begin before age 20. Epigastric pain and ( pancreatic enzymes. Symptoms may be mild, or may appear as acute or chronic pancreatitis.
Abd radiographs ( calcification in approximately 50% of pts.
There is ( risk of pancreatic cancer ( ~ 40% risk by age 70.
Mutation in the cationic trypsinogen gene on Ch 7 ( abnormality in the trypsinogen molecule which inhibits degradation by trypsin in a feed-back ioop. Under normal circumstances, there is a low level of trypsinogen autoactivation in the pancreas. Any activated trypsin within the pancreas is inhibited by trypsin inhibitor. However if there is excessive trypsin activation which exceeds the amount of trypsin inhibitor, then trypsin can feedback on itself and hydrolyze trypsin to prevent activating the cascade of pancreatic enzymes. In patients with hereditary pancreatitis, activated trypsin will not be inactivated, and therefore will lead to generalized digestive enzyme activation leading to pancreatitis.

Transitional Diets posted by Robin H

2006-01-13T03:18:00.000+10:30

Robin H found this for transitional diets for Pancreatitis
PANCREATITIS MESSAGE BOARD
Posted by cj on December 30, 2005 at 18:53:09:
I just couldn’t get the daily example of diet to space right, so it was just choices off the lists below.

Transitional Diets for Pancreatitis

When you are discharged home from the hospital, you will be starting off with a diet that is easier for your body to tolerate and will not stimulate your pancreas too much.

Gradually, you will be allowed more and more food, and will transition finally to a low-fat regular diet that you can stay on almost indefinitely to minimize pain and abdominal symptoms.

Start off with the clear liquid diet (1), then when you tolerate this without pain, nausea, vomiting or diarrhea, advance to the full liquid diet (2). When you tolerate this, advance to the low-residue low-fat diet (3). Finally, you can graduate to the regular low-fat diet (4).

This transition should be slow to avoid any problems with worsening pain or Pancreatitis symptoms. A rough rule of thumb is to complete the transition from clear liquid to solid, but a low-fat diet, within 1 week. Please remember that the pancreas is more prone to react to fatty (heavy) food and food that stays within the stomach for a long time. Therefore, a liquid diet or a low-fat diet is better tolerated than a solid, regular or high-fat diet.

The following pages will give you some guidance on what to avoid and what to choose during your transition. The last page gives a sample menu for each stage of the diet.

If you have diabetes or are prone to high blood sugars, follow the asterix (*) for extra instructions on how to balance the carbohydrates in your diet.

1. Clear Liquid Diet

The clear liquid diet is used only very short term, for example, 2 to 3 days, for when you are initially starting to eat. This is a very limited diet with only the following items. When you are feeling better, and have minimal abdominal pain, no nausea, vomiting or diarrhea, move on to the Full Liquid Diet (2).Juices*Broth, Clear soups Gelatin (Jell-O),*Sorbet*

Popsicles*, Fruit ices*, 7-up or Sprite*, Sports drinks such as Gatorade*
* if you have diabetes or are prone to high blood sugars, have at least two but not more than three 4-oz portions of these carbohydrate containing clear liquids at each meal. You can have unlimited diet gelatin (diet Jell-O), Diet 7-up or Diet Sprite, or diet fruit ices in addition.

2. Full Liquid Diet

When you are ready to add to the Clear Liquid Diet, add the following items to your diet, and continue to have everything allowed on the Clear Liquid Diet. Make sure you try to eat at least 3 times a day to try to meet your nutritional requirements. You should not follow this diet for more than 2 weeks as it is not fully nutritionally adequate. When you tolerate this diet, move on to the low-residue, low-fat diet.
Milk*Smooth yogurt with no fruit chunks*, Broth soup, Cream soup*, Pudding*, Custard*, Low-fat Ice cream*, Boost or Ensure*, Fruit smoothies*, Rice milk*, Soy milk*

* if you have diabetes or are prone to high blood sugars, have at least two but not more than three 4-oz portions of these carbohydrate containing clear liquids at each meal. You can have unlimited diet gelatin (diet Jell-O), Diet 7-up or Diet Sprite, or diet fruit ices in addition.

3. Low Residue (Low-Fiber), Low-Fat Diet

A low-residue or low-fiber, low-fat diet avoids most foods with a lot of fiber and fat. Try to consume white breads, white rice, and not too many raw fruits or vegetables. Avoid fatty foods. This will allow you to transition to a regular low-fat diet more easily, and minimize pain and other symptoms such as nausea, vomiting and diarrhea. This diet is balanced and can be followed for weeks.

L Foods to AVOID:

Whole grain and whole wheat breads , Rye breads with seeds ,Nuts and seeds , Granola and granola bars , Dried fruit , Coconut , Raw fruits , Raw vegetables
Salads:
Gas-producing vegetables: Broccoli, Brussels sprouts, Cabbage, Cauliflower Sauerkraut, Onions, Vegetables with seeds:, Eggplant. Tomatoes Fried meats , Tough meats , Sausages , Bologna , Peanut butter , Beans , Jams and preserves , Fried potatoes/french fries , Wild or brown rice , Whole wheat pasta , Ice cream , Cream , Butter , Pudding , Coffee , Gravy , Mayonnaise

J Foods to EAT:

White breadSourdough breadEnglish muffins, Pancakes and waffles, Canned fruit (moderation), Crackers, Cream of wheat, Oatmeal, Soft cooked vegetables: Asparagus tip, Carrots, Beets, Green beans, Spinach, Summer squash, Zucchini, Mushrooms, Soft fruits (limit 2 per day): , Melon, peach, banana, or skinless, Tender lean meats, Skinless chicken, Fish, Turkey, ground turkey, Jelly, Honey, Mashed potatoes , Baked potatoes no skin, Boiled potatoes, White rice, noodles, Pasta (not whole wheat), w-fat milk (if tolerated)Lactaid milk, yogurt, Angel food cake, Fruit juices, soy milk, Lite mayonnaise

4. Low-Fat Diet

A low fat diet is the recommended diet to follow almost indefinitely when you have Pancreatitis. Try to follow a low-fat diet consistently, eating no more than 50 grams of fat per day. A low-fat diet is a balanced, healthy way to eat
L Foods to AVOID:
Croissants , Donuts, muffins , Nuts and nut butters , Granola and granola bars Cakes, cookies , Oily crackers (e.g. Ritz) , Bacon and eggs , Cream soups , Salad dressings , Croutons , Bacon bits , Sour cream , Sesame and other seeds , Fried meats , Fatty meats , Sausages , Cheeseburger , Bologna, hot dogs , Peanut butter Cheese , Mayonnaise , Fried potatoes/french fries , Scalloped potatoes , Pasta with cream sauce , Ice cream, Cream , Fried noodles, Pudding , Pound cake, cakes with icing , Cookies

J Foods to EAT:

White or wheat bread, Sourdough bread, rye bread, English muffins, pancakes, waffles, Corn flakes, rice crispies, cereal bars, Fresh fruit, dried fruit, juices, Dry crackers, e.g. soda, graham, water, Cream of wheat, oatmeal, , Vegetable soups, broth based soups , Salads, vegetables, fat-free dressings, Vinegars, Garbanzo beans, Plain yogurt, nonfat sour cream, Pretzels, Skinless chicken , Lean meats, Ham, roast beef, roast turkey slices, Turkey burger, no cheese, “Smart Dogs” and other soy products, Turkey, ground turkey, Jams and Jelly, Mustard, ketchup, lite mayo, Mashed potatoes with no butter, Baked potatoes, boiled potato, Pasta with tomato based sauce, Sorbet, sherbet, low-fat frozen yogurt, Low-fat desserts , Noodles in soup, Nonfat or low-fat milk or yogurt, Angel food cake, All fruits

FREQUENTLY ASKED QUESTIONS ON PANCREATITIS DIET

1. What kind of diet do I have to follow for life?

The kind of diet that is best for someone with chronic Pancreatitis is a diet that is low in fat, low in sugar, and moderate in protein. That means, most of your diet will consist of fruits and vegetables, lean meats, skinless chicken and turkey, fish, potatoes, rice and pasta, and low-fat dairy products and soy. This is similar to the diet recommended for patients with heart disease, so you can look in bookstores for cookbooks for heart-healthy diets, and you can choose items on restaurant menus that are intended for heart-healthy diets.

2. Can I follow a low-carbohydrate, Atkins-type diet if I have Pancreatitis and want to lose weight?

A low-carbohydrate, Atkins-type diet will probably have too much meat and fat for a person with Pancreatitis to follow. However, it is important for a person with Pancreatitis to eat enough protein. The best is to be moderate in your protein intake and try to avoid fatty meats and fatty food preparation techniques such as frying and sautéing.
In general, it is not advised to follow an Atkins-type diet if you have Pancreatitis. If you wish to lose weight, cut down on foods with a lot of calories, such a juices, sweets, baked goods, heavy sauces, and reduce your portion sizes of rice, bread, pasta, and potatoes. Don’t cut them out entirely, as they are low-fat foods. Eat more vegetables. Make sure you eat breakfast (this actually helps with weight loss). Make sure you do some exercise daily or every other day for at least 30 minutes. It can be walking or any activity you enjoy and can do consistently.

3. How much protein do I need per day?

Most adults need about 6 oz of fish, chicken, turkey, or lean meat every day. You can divide this into 3 oz at lunch and 3 oz at dinner, or 2 oz at lunch and 4 oz at dinner. A 3 oz portion is the size of a deck of cards. A 4 oz portion is about the size of a woman’s palm. A slice of turkey or chicken is about 1 oz, so a sandwich with 2 slices is about 2 oz of protein food.
Eating enough protein is important. Don’t cut out all protein foods.

4. What if I’m vegetarian?

If you are vegetarian, you need to obtain your protein from beans, soy products, eggs, and dairy products. Try not to use cheese and nuts for protein, as they come with a lot of fat also. Instead, purchase a low-fat vegetarian cookbook and make items such as bean chili, tofu stir-fries (with a minimum of vegetable oil), and other such vegetarian recipes. Low-fat milk, eggs, yogurt and cottage cheese are also acceptable sources of protein.

5. What are some things I can snack on?

Low-fat snacks include fresh fruit, fruited yogurt, low-fat crackers, cereal and milk, liteJell-O, toast and jam, or bagel.

6. Should I avoid sugar?

If you have high blood sugars, you may need to be on a diabetic diet. It is best, then, to avoid sugar as much as possible, but also be aware of your portion sizes for starchy foods such as rice, potato, pasta, bread, cereal, and noodles. Keep your portions sizes to ½ to 1 cup per meal, and only have one of these starchy items per meal. Eat more vegetables instead.

If you don’t currently have high blood sugars, you can have some foods with sugar, and use small amounts of sugar in foods and beverages, but be moderate. The reason for this is that the pancreas is responsible for making insulin, the hormone that helps the body utilize sugar, so if your pancreas is stressed, it may be stressed further if you constantly eat a high sugar diet. Use sugar and sweets in moderation.

Newbie Post 0

2006-01-13T01:19:00.000+10:30

Newbie 0: Define the diseases, Acute vs. Chronic
PANCREATITIS MESSAGE BOARD
Posted by Chuck on September 28, 2004 at 11:29:17:

Chronic Pancreatitis versus Acute Pancreatitis.

Let's start with definitions since they are vastly different diseases. Acute Pancreatitis is defined as an inflammation of the pancreas. That's all. Chronic Pancreatitis is a progressive, incurable disease defined as permanent structural damage to the pancreas. Pretty simplistic definitions aren't they? Too bad that with definitions so broad they still cannot diagnose them quickly and easily.
Acute Pancreatitis can be caused by excess (and activated) pancreatic enzymes within the pancreas, alcohol abuse, blunt force trauma, pancreatic duct obstruction or even medications. It can manifest itself as acute (temporary) abdominal pain, nausea, diarrhea and fever. It can sometimes be determined by elevated serum levels of the pancreatic enzymes, amylase (unreliable measure) and lipase (more reliable than serum amylase but may be useless after 24-48 hours after initial onset). Acute Pancreatitis is very dangerous since high amylase and lipase levels may compromise the heart, lungs, liver, spleen and kidneys.
Acute Pancreatitis may show up as "subclinical", small relatively minor inconveniences like a daily case of diarrhea after lunch or a particular burning under your ribcage after dinner. It can range all the way up to life threatening, debilitating, severe attacks which require hospitalization. Most Acute Pancreatitis patients make a complete recovery within a few days to a week of their attack and will never have another one if the main antagonist (alcohol, drugs, obstructions, etc.) is removed from the patients life.
Chronic Pancreatitis is an enigma to most. It is a very rare disease and only occurs in 8.5 out of 100,000 population (.0085%) in the US. The mechanism of pain and dysfunction is not understood by today's medicine. There are no generally accepted diagnostic or treatment methods. Every Doctor has his/her own "favorite" out of a limited number of studies done. As a result successes are few even when success is defined as slowing the deterioration of the organ or giving temporary relief from the pain.
While Acute Pancreatitis attacks can and sometimes do cause Chronic Pancreatitis the disease are as different as night and day.

Chuck

Newbie Post 1

2006-01-13T01:18:00.000+10:30

Newbie 1: What is Chronic Pancreatitis?
PANCREATITIS MESSAGE BOARD
Posted by Chuck on September 28, 2004 at 11:30:13:

This is the second of a series of messages that I repost occasionally as we get new people. I hope they are of some help.
In normal conversation the Docs I worked with throw around a few terms that have no specific definable borderlines. Chronic Pancreatitis by definition is the result of unrecoverable structural damage to the pancreas. Period. Nothing fancier than that. So you can imagine what Doctors, who are supposed to be scientists, do when presented with such a broad definition as that. What tissue defines structure? Is it exocrine or endocrine structure? Where does it have to be damaged? How much damage?

Early Chronic Pancreatitis is what they use when they don't know how much damage there is but you show several of the symptoms. This is usually only used until they determine what is really wrong. The mistake many patients make is to let them get away with this definition. Make them define the type of damage that has been or is being done.

Damage to the pancreas can be diffuse, focused or annular. Diffuse or sclerosing damage is the hardest for the Docs to deal with because they can't point at something and go "A-HA". Since there is no single point of failure it is usually written off as "idiopathic" or no known cause. The deterioration is unpredictable in speed but the progress is steady and frequently accelerating. The pain from this form is just as steady and unrelenting. It can be mild or severe but since it never stops or even slows down it is simply mind numbing. Depression is extremely common among these patients due to the unrelenting nature of the chronic pain
Focused damage to the pancreas is almost never labeled idiopathic. There will almost always be an obstruction or defect at the root cause. Obstructions can be a stone, tumor, stricture or malfunctioning valve (SOD). Defects that can be at the core of focused damage include Pancreas Divisum, blood flow restrictions and several very rare conditions. Unless the root cause is fixed/removed the deterioration is usually very rapid and excruciatingly painful. The pain tends to come in peaks and valleys. The longer the obstruction remains in place, the more damage is done, the higher the baseline level of pain becomes. Surgery is very often determined to be an answer for patients with focused damage. If the surgery is early enough then it is highly successful and the patient may never show another symptom. The later in the deterioration it is done, the lower the odds of success.

Damage known as Annular Pancreas is very rare. In this type the damage basically forms in a ring. As the ring dies and becomes larger it can cut off or strangle sections of the exocrine pancreas behind it. This can go unnoticed until it is too late. You can end up losing a huge amount or all of the pancreas very rapidly. The pain usually doesn't become severe until it is very advanced. A very complicated surgery is almost always required. Many times a Whipple is the only answer if there is any hope of being pain free and insulin independent.
You'll hear the docs throw around the terms mild, early, severe and end-stage casually. Doctors that throw around the term mild should probably be fired. How can you have irrecoverable damage to a critical organ and have it be "mild"?
The best way I can tell to categorize CP is by defining early as the stage you're in before they figure out how much damage has really been caused and what the root is. Middle stage is while all of the symptoms are manageable by diet/lifestyle changes or medication and you can still function in your normal life completely. This doesn't mean you are not going to have acute attacks or flare-ups. It just means that your day to day life can go on with little modification.
Severe CP begins when medication is unable to control one or more of the symptoms on a regular basis. Your life has a severe impact as you are unable to perform to the degree you had in the past. Severe CP is more a state of symptoms than it is a measurement of quantity of damage.
End-stage is just what it sounds like. The structure of your pancreas has deteriorated to the point of near or complete exocrine dysfunction. Pain is disabling and enzyme supplements are required for even the smallest amount of food. At this point it is possible that the damage has caused irreparable harm to the Islets of Langerhans. Islet cells produce insulin into small pools in the Isles where it is picked up into the blood stream. If the damage has compromised the blood flow or has caused too many of the cells or pool locations to become non-functional then diabetes can occur. Doctors will bring up a complete pancreatectomy for pain control if there is little hope for retention of insulin independence.

There is a stage that may be the medical equivalent of an Urban Legend. Burnout is the stage where all exocrine cells have been destroyed by the disease. Since there is no more to deteriorate, the pain stops. Enzyme supplements are required but they probably have been a requirement on the table of the CP patient for a long time anyway. Although there is some argument internationally the Doctors here believe it is highly likely that diabetes will result. Still, there is that ray of hope to cling to.

"Pain free and insulin independent" is the last dream of the CP patient.
I was told by my Surgeon not to have the Total Pancreatectomy that my GI Doctor had recommended. When a Surgeon tells you not to get cut you have to listen. The fact that he is the Head of the Surgery Department AND the Islet Transplantation Center at one of the top medical schools in the country gives him instant credibility. He also was the Doctor who performed the Whipple Procedure on me.
He said that we are within 5-10 years of some remarkable breakthroughs in Endocrinology and Transplantation that may change our perceptions completely. That was in 1999 and there are several still on the horizon. Geneticists are rapidly closing in on raising pigs with no genetic rejection markers. Your immune system would not recognize it as a foreign body when transplanted. This would give us a virtually unlimited supply of hearts, livers, pancreii and kidneys available for transplantation without the harsh life with anti-rejection drugs.
There are also promising technique modifications in the works for harvesting a larger number of Islets from a pancreas during a Pancreatectomy with Islet Cell Auto Transplant. That might make more of the procedures fully successful.
Living without a pancreas is no picnic and Dr. Brunicardi would have to be convinced that there was no hope before he would take out a non-cancerous pancreas.

Anytime a Doctor starts taking about cutting the first thing to ask is which surgery the doc has in mind. There are only a few choices. There are endoscopic procedures done under the auspices of an ERCP. They can open up the sphincters by cutting them with a wire lead or placing stents or both. All of the other procedures are open surgeries.

There is a Puestow procedure which basically is used for ductal problems. They filet the pancreas and sew it directly into the duodenum so the pancreas secretes directly into the small intestine. There is very little tissue that is discarded in the process.

The other commonly available surgery is the Whipple procedure. This is very major surgery. There are a million options on this one. Questions to be determined are how much will be removed, which part will be taken and how many Whipples has the doc done. There are also differing techniques. My surgeon used a technique he helped refine when he was at UCLA. He has actually done hundreds of them. He saved both my pylorus and the duodenum. He removed my gall bladder, 3/4 of my pancreas and 1/2 of my stomach. There is another variant called a Beger Procedure that reduces recovery time even more as it saves more if not all of the stomach along with the pylorus and duodenum. This is a relatively new procedure in the US but has been used in Germany for quite a while.
The complications of these surgeries can be bleeding, infection or fistula (leakage). The location and number of drains (Jackson-Pratt) to remove leakage has a definite impact on the time it takes to recover. I was out of the hospital in less than 2 weeks and had my single drain removed after 3 weeks. Recovery is completely based upon the skill of the surgeon and what he/she finds once you're opened up.

There is an experimental surgery that is available in very few locations with the most notable being the University of Minnesota Fairview Hospital. The Total Pancreatectomy with Islet Cell Autotransplant removes the pancreas, smushes it up and turns it into slurry, isolates the insulin producing Beta cells and injects them into the portal vein where they take up residence in the liver. The Beta cells will hopefully continue to produce insulin and will be absorbed into the bloodstream just as if they were still in their original place. The harvesting process can sometimes be very inefficient. There is no way the surgeons can tell you ahead of time if they will be able to harvest the 300,000 islet cells that are necessary to have full insulin function. Also if the nerve root has been damaged by the deterioration of the pancreas the pain may not go away with the pancreas. There is a very real possibility that you could go through this $125,000 operation and be a brittle diabetic who still has intractable pain. That is why most insurance companies still do not cover the procedure.

There are a few variations of these surgeries such as a distal Pancreatectomy where they remove the tail of the pancreas and leave the head. This is a relatively easy surgery for the surgeon since there are no blood supply issues. It is simply removing diseased or necrotic tissue. Recovery is usually very quick. I don't want anyone to think I am trivializing this surgery. It is still major surgery of the Alimentary and Endocrine Systems of the body. It is just that complications are few and recovery is fast. The outcome is usually that the patient becomes a type 1 diabetic (insulin dependent).

There is another surgery that is once again pretty major. It is basically opening you up and surgically cutting open the pancreas to widen the end of the ducts and the sphincters so that the pancreas will drain better. The pancreas doesn't like to be fooled with like this and the initial result is severe acute Pancreatitis. Once the attack is controlled the flow should be back to what a non afflicted person considers normal. The biggest complications come when the duct forms scar tissue and/or re-stenoses. That makes the first surgery moot and leaves you in the position of needing a Whipple because of the damage done.

Occasionally, when the pancreas cells rapidly die off in massive numbers they cannot be sloughed out fast enough. Instead of being passed out of the pancreas along with bile and enzymes they collect in what for all extents and purposes is a balloon of tissue called a pseudocyst. Usually these containers of necrotic tissue dissipate on their own. If they do not then surgery is required.
There are two main types of intervention to pseudocysts. The first is minimally invasive. Guided by an Endoscopic Ultrasound (EUS) they guide a fine needle into the pseudocyst and drain it with a syringe. This is called fine needle aspiration. I have never heard of anyone having a pseudocyst of any large size, say 7 cm or larger, successfully drained by fine needle aspiration.

Once a pseudocyst starts to get to a point of danger, either from compromising other organs or fear of rupturing, then more drastic methods must be used. A drain is placed surgically to remove the fluid into either the stomach or small intestine. In extremely rare cases it is drained into the pancreas or the large intestine. Regardless it is not fun either way. Pseudocysts are very painful, upsetting and dangerous.

If it sounds like pancreatic surgery is all desperate measures for desperate people then you probably understand perfectly. From an ERCP to the Whipple or even a complete Pancreatectomy it is all done because we so very desperately want the pain and the nausea and the pain and the diarrhea and oh, yeah, the pain to just stop.

Hopefully, this gives you a little bit to talk to your surgeon about. I can't help in any way to steer you to one or the other. Each has it's own justification. Just have the doc tell you why or why not on each.

Chuck

Newbie Post 2

2006-01-13T01:15:00.000+10:30

Newbie 2: How do I live with this accursed disease?
PANCREATITIS MESSAGE BOARD
Posted by Chuck on September 28, 2004 at 11:31:08:

I would love to give you good news about Chronic Pancreatitis but I can't. Today it is still an incurable progressive disease. Doctors can give you prescriptions to help give you some relief from individual symptoms. The big key to the future of CP patients are NO ALCOHOL WHATSOEVER, low fat diet, keep triglycerides down if possible, get good GI & Pain Management docs, take your enzyme supplements religiously (I mean all the time, every time, not to pray over them altough I think that would also help sometimes) and don't try to be brave and tough out your pain - take your pain meds whenever you have pain, period (if you have pain all the time DO NOT miss a dose at all). Let someone else worry about addiction. You worry about covering your pain.

Let's face it. Our quality of life is totally dependent upon our conformance to these principals and the quality of our doctors. If you have a Doctor (with a Capital "D") that has great knowledge of pancreatobiliary diseases and compassion for your condition and admit when he/she is over his/her head and will call for help when needed you will probably have a better quality of life than if you have one of the thousands of doctors (small "d") that either are ignorant, arrogant or apathetic (some can fit into all 3 categories). We refer to these people as DINKs (Doctors In Need of Knowledge).

We highly recommend keeping a food and event diary. This journal can help you find your triggers and limits. Sometimes this disease can be fickle and hurt you one day for something that was fine the week before but as a general rule what hurts us once has a tendency to hurt us again. The diary can remind you of what you did or ate before each attack. You can also keep your questions for the doctor in it. Then make sure you take your journal with you to every appointment.
Hang around here for a while. You are among friends who know exactly what you are going through. We welcome you with open arms. Feel free to ask any questions you want. You would be very surpised at some of the topics we get into. Some are funny, some are gross but we are very much like a family here so anything goes.

Chuck

Newbie Post 3

2006-01-13T01:14:00.000+10:30

MESSAGE BOARD.
Newbie 3: Grieve for your lost health and lifestyle
PANCREATITIS MESSAGE BOARD
Posted by Chuck on September 28, 2004 at 11:32:36:

We all have to go through the 5 stages of grief many times in our lives. One of the most important for us is to grieve for our lost lives and lost health. A diagnosis of Chronic Pancreatitis takes away so many things from our lives. The most critical of them is hope. We need to grieve for the loss of our "life as we know it".

Five Stages of Grief

The first stage is denial
Upon hearing the diagnosis, the patient reacts with a shocked, "No, not me." According to Dr.Kubler-Ross, this is a healthy stage, and permits the patient and the family to develop other defenses.
Next comes anger or resentment
"Why me?" is the question asked now. "Why my child?" Blame, directed against the doctor, nurses and God often is a part of this stage. This outcry should be accepted, unjudged.
The third stage is bargaining
"Yes me, but-" "If you'll just let me/him/her be well, God, I'll . . ." This Dr. Kubler-Ross calls a period of temporary truce.
The fourth stage is depression
Now the person says, "Yes, me," with the courage to admit that it is happening; this acknowledgment brings depression. (Note: The family often goes through all the stages, along with the patient.)
Finally comes acceptance
A time of facing serious illness or death calmly. This is often a difficult time for the family, since the patient tends to withdraw, to be silent.

Chuck

Newbie Post 4

2006-01-13T01:12:00.000+10:30

Newbie 4: How to successfully navigate the ER
PANCREATITIS MESSAGE BOARD
Posted by Chuck on September 28, 2004 at 11:33:42:

Regularly, CP patients are turned away from Emergency Rooms because their serum amylase/lipase numbers are not elevated. The DINKs (Doctors In Need of Knowledge) are unaware that Amylase can return to WNL (Within Normal Limits) in as quickly as 12 hours after onset (or less in the case of Sphincter of Oddi Dysfunction) of an acute attack. Even the slower to react serum lipase levels can return to WNL in 24-48 hours.
Basically an acute attack is a chemical burn on the inside of your pancreas. Does a burn stop hurting when the flame is removed from the skin? If you had spilled Sodium Hydroxide (NaOH - a very strong base reagent) on your skin would they pat you on the head, give you a Tylenol and snicker behind your back as they sent you home untreated? Of course not but that is exactly what they do regularly for CP patients who have an equally painful chemical irritation to their pancreas.
I suggest carrying a letter with you explaining to the ER DINK exactly what your situation is. Make sure you carry a list of all medications, your insurance information and all the contact info for your GI Doctor.

Here is what I carry. I suggest you come up with one as well

[Personal contact information] [List of Medications, Dosages & Why taken]
[Insurance information]
[GI Doctor name address and phone number]

If you have been given this letter it is because I have landed in your Emergency Room. I am not a junkie or a drug seeker. I suffer from severe Chronic Pancreatitis. I am on pain medication 24x7. All of my medications are listed above. Chronic Pancreatitis leaves me fighting without cessation the worst imaginable pain. If I am here it is because the medications I have are not enough to make me tolerate the pain.
Since I suffer from Chronic Pancreatitis it is possible for me to be suffering from an Pancreatitis flare up without having extreme elevations of my pancreatic enzymes (amylase and lipase). Please contact my Gastroenterologist, [enter your GI docs name and telephone number here] if you have any questions about my condition.
[Enter your GI doctors instructions here]

For me an Chronic Pancreatitis flare up usually presents itself as uncontrolled nausea including repeated vomiting and extreme upper abdominal pain presenting itself as a high level (5-7) of constant pain with surges of breathtaking pain (8-9).
As a warning, I am a very "tough stick" when it comes to finding a vein for an IV. Pancreatitis and the huge number of IV’s I have had in my life have ruined my veins. Most of the IV’s that are put in the ER blow out within hours. If I am to be admitted I request that you put in a central line.
I carry this letter because many people with Pancreatitis are sent home without treatment from Emergency Rooms because some tests return WNL. Many Doctors, interns and med students are not knowledgeable of Acute or Chronic Pancreatitis and jump to the conclusion that the patient is seeking drugs or even just attention. I understand there are only 5-10 cases of Pancreatitis that show up each year per 100,000 population and only 2.72 cases of Chronic Pancreatitis are discovered. I know that you do not see many people with my condition and you see many more drug seekers than Pancreatitis sufferers. Please understand that my pain and other symptoms are real and I do indeed need treatment, even if it is only IV fluids and pain medication.
Thank you for your understanding.

Newbie Post 5

2006-01-13T01:10:00.000+10:30

Newbie 5: NEVER, EVER self diagnose
PANCREATITIS MESSAGE BOARD
Posted by Chuck on September 28, 2004 at 11:34:32:

Last of all for the usual disclaimer.

As the boards resident amateur biologist I do have to warn you about self diagnosis. For every symptom we can come up with there are literally hundreds of possible causes. We tend to hone in on a single symptom until we find one that fits. A doctor can't get away with that. Our research can however help push the docs into action. It can help get them to test you for certain diseases/syndromes. We have to be careful and believe them with healthy skepticism when they tell us no. We must accept a no answer but it must be just a step in finding a true diagnosis. There has to be more to it than just no. Accept it but push for a diagnosis.
The doctors have an old worn out saying "If you hear hoof beats think horses not zebras". It basically means to look for the most common of causes of the symptoms before seeking out the rarer ones. Chronic Pancreatitis is extremely rare. The last reports we have seen put the incidence in the United States at about 8.5 patients per 100,000 population. That is why most doctors see few if any cases of Chronic Pancreatitis in their careers.
IMHO you have to let the process work out to it's final end. You just need to make sure the docs don't stop the process short. Don't accept a default diagnosis. Make sure you get a definitive one.
This even extends to new symptoms as they arise. CP patients have leaned to live with pain that would have others writhing on the floor. As such we tend to downplay new symptoms as they show up. We rationalize that it is a normal part of the disease and just live with it. This is a passive form of self diagnosis.
Make sure when you get new issues that you let your doctor/Doctor know about it. That one symptom may be the key to discovering why you continue to have flare ups or attacks.

Chuck

Symptoms for newbies

2006-01-13T01:03:00.000+10:30

Symptoms for newbie’s
PANCREATITIS MESSAGE BOARD
Posted by cj on September 27, 2004 at 21:45:47:

Do you all remember when we all figured out we all had the same referred shoulder pains? or some other symptom? I was chatting with a lady at the salon I work at and her hub might also be suffering from panc or maybe gallbladder. She brought up the right hand shoulder pain, and also the horrendous sweats. I can remember when we found and when others find this site and are like OMG i'm not alone!! we all have similar symptoms be it from, acute panc/chronic panc/alcoholic panc/idiopathic panc/ panc caused by meds/viruses ECT! scary how more and more people are showing up with this disease. I sent her this link and hope she shows up and can read and see if maybe hub has same issues. I know how nice everyone is and will help out.

A Letter to Normals

2006-01-13T00:48:00.000+10:30

A Letter to Normals from a Person With Chronic Pain

Having chronic pain means many things change, and a lot of them are
invisible. Unlike having cancer or being hurt in an accident, most
people do not understand even a little about chronic pain and its
effects, and of those that think they know, many are actually
misinformed.

In the spirit of informing those who wish to understand:
These are the things that I would like you to understand about me
before you judge me.

Please understand that being sick doesn't mean I'm not still a human
being. I have to spend most of my day in considerable pain and
exhaustion, and if you visit, sometimes I probably don't seem like
much fun to be with, but I'm still me, stuck inside this body. I
still worry about work, my family, my friends, and most of the time,
I'd still like to hear you talk about yours, too.

Please understand the difference between "happy" and "healthy". When
you've got the flu, you probably feel miserable with it, but I've
been sick for years. I can't be miserable all the time. In fact, I
work hard at not being miserable. So, if you're talking to me and I
sound happy, it means I'm happy. that's all. It doesn't mean that
I'm not in a lot of pain, or extremely tired, or that I'm getting
better, or any of those things. Please don't say, "Oh, you're
sounding better!" or "But you look so healthy!" I am merely coping.
I am sounding happy and trying to look normal. If you want to
comment on that, you're welcome.

Please understand that being able to stand up for ten minutes
doesn't necessarily mean that I can stand up for twenty minutes, or
an hour. Just because I managed to stand up for thirty minutes
yesterday doesn't mean that I can do the same today. With a lot of
diseases you're either paralyzed, or you can move. With this one, it
gets more confusing everyday. It can be like a yo-yo. I never know
from day to day, how I am going to feel when I wake up. In most
cases, I never know from minute to minute. That is one of the
hardest and most frustrating components of chronic pain.

Please repeat the above paragraph
substituting, "sitting", "walking", "thinking", "concentrating", "bei
ng sociable" and so on, it applies to everything. That's what
chronic pain does to you.

Please understand that chronic pain is variable. It's quite possible
(for many, it's common) that one day I am able to walk to the park
and back, while the next day I'll have trouble getting to the next
room. Please don't attack me when I'm ill by saying, "But you did it
before!" or "Oh, come on, I know you can do this!" If you want me to
do something, then ask if I can. In a similar vein, I may need to
cancel a previous commitment at the last minute. If this happens,
please do not take it personally. If you are able, please try to
always remember how very lucky you are, to be physically able to do
all of the things that you can do.

Please understand that "getting out and doing things" does not make
me feel better, and can often make me seriously worse. You don't
know what I go through or how I suffer in my own private time.
Telling me that I need to exercise, or do some things to "get my
mind off of it", may frustrate me to tears, and is not correct. if I
was capable of doing some things any or all of the time, don't you
know that I would? I am working with my doctors and I am doing what
I am supposed to do. Another statement that hurts is, "You just need
to push yourself more, try harder". Obviously, chronic pain can deal
with the whole body, or be localized to specific areas. Sometimes
participating in a single activity for a short or a long period of
time can cause more damage and physical pain than you could ever
imagine. Not to mention the recovery time, which can be intense. You
can't always read it on my face or in my body language. Also,
chronic pain may cause secondary depression (wouldn't you get
depressed and down if you were hurting constantly for months or
years?), but it is not created by depression.

Please understand that if I say I have to sit down,lie down, stay in
bed, or take these pills now, that probably means that I do have to
do it right now, it can't be put off or forgotten just because I'm
somewhere, or I'm right in the middle of doing something. Chronic
pain does not forgive, nor does it wait for anyone.

If you want to suggest a cure to me, please don't. It's not because
I don't appreciate the thought, and it's not because I don't want to
get well. Lord knows that isn't true. In all likelihood, if you've
heard of it or tried it, so have I. In some cases, I have been made
sicker, not better. This can involve side effects or allergic
reactions, as is the case with herbal remedies. It also includes
failure, which in and of itself can make me feel even lower. If
there were something that cured, or even helped people with my form
of chronic pain, then we'd know about it. There is worldwide
networking (both on and off the Internet) between people with
chronic pain. If something worked, we would KNOW. It's definitely
not for lack of trying. If, after reading this, you still feel the
need to suggest a cure, then so be it. I may take what you said and
discuss it with my doctor.

If I seem touchy, it's probably because I am. It's not how I try to
be. As a matter of fact, I try very hard to be normal. I hope you
will try to understand. I have been, and am still, going through a
lot. Chronic pain is hard for you to understand unless you have had
it. It wreaks havoc on the body and the mind. It is exhausting and
exasperating. Almost all the time, I know that I am doing my best to
cope with this, and live my life to the best of my ability. I ask
you to bear with me, and accept me as I am. I know that you cannot
literally understand my situation unless you have been in my shoes,
but as much as is possible, I am asking you to try to be
understanding in general.

In many ways I depend on you, people who are not sick. I need you to
visit me when I am too sick to go out. Sometimes I need you help me
with the shopping, the cooking or the cleaning. I may need you to
take me to the doctor, or to the store. You are my link to
the "normalcy" of life. You can help me to keep in touch with the
parts of life that I miss and fully intend to undertake again, just
as soon as I am able.

I know that I asked a lot from you, and I do thank you for
listening. It really does mean a lot.

Adapted from a work by Bek Oberin

2006-01-05T10:46:00.000+10:30

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