This is quite possibly your ONLY chance toask “Live” questions to one of the world’s leading TP/AIT (transplant) surgeon!
JAN 2nd, 2009 - CaseyAnne & Dr. David E. R. Sutherland
Diabetes-Pancreatitis Breakthrough!
Awareness Night - Webinar! Thursday, November 17, 2011 @5pm PST
Presented by Dr. David Sutherland and Dr. Melena Bellin.
Live Q & A by the world renowned surgeon Dr.David Sutherland & Dr. Melina Bellin.
Casey has had them both, with Dr. Bellin removing her blood clot- the size of a lemon- PLUS over 2 LITERS of blood and other fluid from her abdomen- (This was 10 days after her TP/AIT). Please CLICK HERE to read that blog. or do the click www.flintville.multiply.com/journal/item/721/UPDATE_IN_COMMENTS_More_Surgery..._More_Prayers...
The Diabetes-Pancreatitis Breakthrough Awareness Night "One of the world's leading transplant surgeons, Dr. David Sutherland who performed the first living donor partial pancreas transplant in the world in 1979, will be the feature guest speaker at the Diabetes-Pancreatitis Breakthrough Awareness Night.
This is an educational event for not only for adults & children who have pancreatitis, diabetes or low blood sugar; but also for medical professionals, caregivers, friends and families who are interested in learning more about the treatment options for pancreatitis and diabetes. CLICK HERE to register.
Dr. David Sutherland, transplant surgeon and Dr. Melena Bellin, pediatric endocrinologist, will be explaining the latest and most innovative technologies to improve quality of life for patients affected by pancreatitis and diabetes. They will explain the before and after process of an islet cell transplant via an online webinar and will answer questions "LIVE!"
Please click on my "Sutherland" tag to read more about him.
*Photo of CaseyAnne with Dr. Sutherland taken only 4 days after her 2nd surgery (abscess)!!
"I'm right there in the room, and no one even acknowledges me"
Kind of long, but very important...
Good Morning. How much further away from what I actually wrote do/can these people go?
Rude. Ignorant. I was called those names... Not to mention that yesterdays post (CLICK) even brought out one recovering alcoholic and drug abuser, on the pancreas site, who took offense. (Was I horning in on his territory with my own assessment of the drug situation at hand)? He claimed there is a difference between addict and dependent (upon).
There is. But his definition was all bass~ackwards. (What the heck do they teach these people in AA/NA groups)? Or do they even teach them (that)? Not sure...
I do not mean to be flippant. That was neither my point, nor my opinion. My point was only to (try to) make others aware that denying their children some pain relief from their intractable pain is a terrible thing to do. (And darn close to abuse in my book).
I chose my wording carefully. The word "addict", referring even to Casey, was/is more than appropriate.
Would your own opinions of my post have changed if you would have known the difference? What if your own child had chronic pain? Or would you be a parent who denies pain relief to your child on the basis of "what if", or "what will the neighbors think?" ?
ADDICTION: compulsive physiological need for and use of a habit-forming substance characterized by tolerance and by well-defined physiological symptoms upon withdrawal; broadly : persistent compulsive use of a substance known by the user to be physically, psychologically, or socially harmful
HABITUATION:
1 : the act or process of making habitual or accustomed 2 a : tolerance to the effects of a drug acquired through continued use, b : psychological dependence on a drug after a period of use—compare ADDICTION 3 : a form of nonassociative learning characterized by a decrease in responsiveness upon repeated exposure to a stimulus —compare SENSITIZATION 3
____
As you can see, the research within the medical guidelines can/will extend past the words above.
Also of vital importance is this: From http://thesaurus.reference.com Notes: "ADDICTION IS MAINLY PHYSICAL WHILE DEPENDENCY IS MOSTLY PSYCHOLOGICAL"
The man in question has since put his tail between his legs (in my opinion) and has stated that he needs to leave the group. Maybe he does. (though I would never write that either).Perhaps his needs would better be served on an AODA site, which I am sure are plentiful. I did say those comments did belong on an AODA site though.
Among other, (nicer) things, I wrote the following: "sadly, your reply only perpetuates all the fears of the people I was addressing. (It also tells me that you have missed the point of my entire posting). I was most certainly NOT writing about ANYthing illegal or immoral. Those were 'your' choices 25+ years ago. The parents, children (and adults) I was writing to/of did NOT have a choice to be part/parcel of a painful disease that needs to be treated."
Note that # 2 definition spells out "DRUG ADDICTION". That's a fact, Sir. You can choose to 'pretty it up' or try to make some off~the~wall comparison, but respect the fact that it won't fly with me.
So he opts to leave. ...Um... er... bu-bye...
Then came woman offended, spouting 'rude' and 'ignorant' (among various other names)- What I would call my "mother image of all things good" -who thought perhaps I did not laud the other guy enough for being clean/sober. My own beliefs are that it is not up to me (or anyone) to pat him on the back. It is up to himself to remain clean/sober. (I did not write that either). Through Roberta's own treatment, she has told me numerous times that I should not censor myself just because she is/always will be recovering. That #1., there is nothing anyone can say/do that will turn her away from clean and sober. That #2., it would be her choice to do so, no matter the circumstances. (That's what she was taught in recovery anyway)...
Anyway, 'XXX' also threw in the idea of Casey, and "pitty parties" (her misspelling, not mine). She further stated "You do NOT know what it is like to suffer day in and day out". (I had to giggle at that one). hehehe
She went on and on- Her prerogative. (I will only copy you on my own reply as I don't think I can copy hers. If you have any questions let me know). But she did say she was sorry if her words hurt my feelings.
My reply, thus...
Dear XXX; Do not worry, xxx, of course you didn't hurt my feelings. I too am an "everyday" person with everyday values and struggles. (We are ALL that, and much more).
You stated, "You do NOT know what it is like to suffer day in and day out" end quote... XXX, I am disabled, and assure you that I can well understand what chronic pain is. But again, this/my story simply does NOT belong on a "pancreatitis" website, (wouldn't you agree)?
Furthermore, I never even broached the possibilities of where that man's disease came from! Quite honestly, that never even crossed my mind until I'd read your note.
Do not attempt to read between my lines. I am quite open and direct.
I believe I tried to make people understand that there are not always "negative" associations with the word 'addict'. I can plainly see you did not interpret our story that way.
My heart goes out to those children (and adults) who will not receive their pain meds because 'someone else' thought they didn't need them, even as prescribed by their doctors!
As I spoke of my own daughter, now 22, (quoted from my original post), "Is she an addict? Yes she is. And in the most humbled definition of the word too." end quote
My words are neither misinformed, nor ignorant.
Nor was I opting for a "pitty party" approach to anything? I know that my Casey would not have lasted through all of her own stuff had she been of a mind to entertain the "pity~pot" mentality. She is much much stronger and wiser than to even attempt to do so. It is her same strength and wisdom that have given me this insight to her own pain.
My apologies (to those who will have to do without), if my more direct approach didn't help you to understand that. As I have just written to the previous poster, "grin and bear it" does not work! (Those words are only for those people who are NOT suffering; for we cannot ever even begin to know another's pain).
Please refer back to the Medical definition of 'dependence'. Note that the # 2 definition spells out "DRUG ADDICTION" in its entirety. I assure you that I did not write that book.
Again, I have tried only to help those who cannot help themselves out of fear (or ignorance) of another.
I believe that through them all (my postings) I have tried to help another out. My apologies (again) if you did not see it that way.
I will close my note to you here exactly as I had closed my first posting [to those parents it applied to]: "Worry less about the pills than you worry about the pain. When that pain is gone then, (and ONLY then), are you/your child to worry about getting away from the pain medicines.
Know that there are no two ways around it. Know too that it doesn't happen overnight. I can only promise that it WILL happen.
Admit that the elephant is in the sitting room. But leave him quietly alone. He will leave in his own time.
Peace and health to everyone during this holy season, whatever your own beliefs are.
Believe in yourself. More importantly, believe in your child." end quote/note
___
One gal wrote that alot of people just don't like the word "ADDICT" ~To whit, (and touché), "a rose by any other name" would apply.
Maybe this will begin to sink in to peoples psyches, and maybe not. I really did try to help these people out.
I have this image of my own 'what if' here... It is the image of my own CaseyAnne, had I ever thought to 'ration' her pills out of fear of what the neighbors would say.
And how, exactly, would I have accomplished that? Would I take her to the doctor, ask for a diagnosis, and then tell him, "Thanks Doc, I'll take it from here." ?
And now, I have images of many kids, much like my Casey, being rationed. Know that it is very hard to get those images out of my mind.
Have a day.
XOXO Anne
PS If you haven't read Part One, please do so. CLICK
"I'm right there in the room, and no one even acknowledges me"
Good Morning All...
I am going to cheat this morning as I have much to do before the dang snow flies. I have written the following to our pancreatitis group. After reading a few messages that dealt with the parents problems. Their failure to give their own children, who are suffering, the doctors prescribed medications; simply because of the negative implications of 'addiction'.
I know there are many children and adults who will not be getting any relief from their pain due to the ignorance of others.
You know me. I call a spade a spade. Read on.
XOXO Anne
************** There is an elephant in the room. You know he is here. Yet we all dance around our replies so very cautiously when we pretend he is not here.
This is my story- Mine, and my daughters.
Having seen CaseyAnne, 22, deal with this illness for 5+ years now, I have also seen her receive massive amounts of drugs to treat it, and the same massive quantities of drugs to keep the pain at bay. (And I learned a very long time ago already that some of the things she has taken would kill a small horse).
It frightened me horribly to see my 4.0 GPA honors student dependent on these dangerous drugs. After all, she is my youngest daughter. She is the one who took the ACT (college aptitude) test at only 11, and received an 18 on it!!! Even Northwestern and Bryn Mawr wanted her after that. The letters, from all over, just kept coming in!
Then came the dx... "Chronic Pancreatitis" I think it was there earlier on in her lifetime, just that we never caught it. Her tummy aches were 'growing pains'. Or maybe she had a bit of food poisoning. Perhaps mittelschmerz.
Whatever, it was, it would pass. Those bouts always did. (Given enough time anyway).
Those tests. The hospitalizations. The flare ups. ALL too numerous to recall offhand. The surgeries that followed, numbering already in the high teens. All these things brought drugs, and more drugs.
Oh my god, my daughter was an addict!
With that thought process came a very profound sense of failure. How would I explain this? Yet if you know me, you will respect that the feeling of failure I had didn't last long. There came a profound sense of compassion, and some very literal understanding.
She NEEDED those drugs to get through an hour, or a day. (And damn what anyone else thought they knew)! She needed those drugs just to live and breathe. Always responsible, she did not take more, (always making an appointment, or a trip to the ER), when she felt it wasn't enough- (Those times she is bent like a question mark, and pain radiates from her features, her sorrowful little body bent, -sad, and twisted).
Casey had her TP/AIT last December. We spent Christmas and January in Minneapolis, so far away from home. Naturally her overwhelming and unrelenting pain was gone.
She recovered from that, only to learn that she had megacolon. In April they removed 70+% of her colon.
She is now facing two more surgeries.
She is still on narcotics, (though she has removed herself from the Fentanyl patch). She is also attending college, and is still receiving great grades. All this, not only because she has a great attitude, she also has a wonderful pain doctor.
Is she an addict? Yes she is. And in the most humbled definition of the word too.
Now about that elephant...
I know there are many parents who are reading this, and who cannot get past the negative images of what an 'addict' is. Get over yourselves already. That addict is your child. That addiction is not negative; it is only the way your childs body has reacted to the only way s/he has to relieve the pain and the suffering.
Keep your priorities in order. When people ask what your child is taking, remember only that it is nobodys business but your own. Remember too that, (if negative in the least), your own gestures, sighs, attitudes, and words can/will offer the greater pain to your child. Your son/daughter has enough to worry about already. Do not put more onto them.
That addict is your son/daughter.
Worry less about the pills than you worry about the pain. When that pain is gone then, (and ONLY then), are you/your child to worry about getting away from the pain medicines.
Know that there are no two ways around it. Know too that it doesn't happen overnight. I can only promise that it WILL happen.
Admit that the elephant is in the sitting room. But leave him quietly alone. He will leave in his own time.
Peace and health to everyone during this holy season, whatever your own beliefs are.
Believe in yourself. More importantly, believe in your child.
XOXO Anne
** Comments are briefly closed. Please comment on following post...
Common variants of the gene that determines human blood type are associated with an increased risk of pancreatic cancer, according to a study by scientists at the National Cancer Institute (NCI), part of the National Institutes of Health, and colleagues from many universities and research institutions. The study, published online Aug. 2, 2009, in Nature Genetics, is consistent with an observation first made more than 50 years ago.
In the study, the researchers discovered that genetic variation in a region of chromosome 9 that contains the gene for ABO blood type was associated with pancreatic cancer risk. Individuals with the variant that results in blood types A, B, or AB were at an increased risk of pancreatic cancer, compared to those with the variant for blood type O. This finding is consistent with previous research, some of it dating back to the 1950s and 1960s, that had shown increased risks of gastric and pancreatic cancer among individuals of the A and B blood groups (i.e., blood types A, B, and AB). The latest results provide a genetic basis for those earlier observations.
A person's blood type depends on which form or forms of the ABO gene they inherit from their parents. The protein produced by the ABO gene determines the type of carbohydrates (complex sugars) that are present on the surface of red blood cells and other cells, including cells of the pancreas. The proteins encoded by the A and B forms of the gene transfer different carbohydrates onto the cell surfaces to make A and B blood types. The O form encodes a protein that is unable to transfer carbohydrates. Studies by other researchers have shown that ABO protein encoding in pancreatic tumor cells is different than in normal pancreatic cells.
To discover genetic variations that contribute to pancreatic cancer risk, the research team conducted a genome-wide association study (GWAS). In a GWAS, researchers analyze common variants, called single-nucleotide polymorphisms (SNPs), in the genomes of people with a disease and people without the disease. Initially, the research team studied the genomes of 1,896 patients with pancreatic cancer and 1,939 control subjects to identify SNPs with a strong association with pancreatic cancer. The team then verified its findings by studying the genomes of another 2,457 people with pancreatic cancer and 2,654 people without the disease. In the end, they identified several SNPs on the long arm of chromosome 9 that were associated with pancreatic cancer risk and mapped to the ABO gene.
"Only by working across disciplines and with more than a dozen research groups were we able to make this important discovery of the potential role of the ABO gene in pancreatic cancer risk," said co-author Patricia Hartge, Sc.D., of NCI's Division of Cancer Epidemiology and Genetics (DCEG). "Although it will take much more work, this finding may lead to improved diagnostic and therapeutic interventions that are so desperately needed."
Pancreatic cancer is the fourth leading cause of cancer death in the United States. It is difficult to detect, and in many people it is not diagnosed until after the disease has spread to other parts of the body. Less than five percent of Americans with pancreatic cancer survive five years past diagnosis. Risk factors include smoking, diabetes, race, and a family history of the disease.
"Pancreatic cancer is the newest beneficiary of so-called high-throughput genotyping that, over the past two years, has yielded scores of genetic hot-spots linked to risk for cancer and other diseases," said co-author Stephen J. Chanock, M.D., chief of NCI's Laboratory of Translational Genomics in DCEG. "As more variants are discovered and follow-up studies are conducted to examine the biological effects of these variants, a better understanding will emerge of the inherited risk factors and mechanisms that lead to the development of pancreatic cancer."
The study was part of PanScan, a GWAS of pancreatic cancer conducted by the Pancreatic Cancer Cohort Consortium, composed of 14 academic centers. The investigators are conducting whole-genome scans to identify common genetic variants that may be markers of susceptibility to pancreatic cancer.
Analyses and data from PanScan will be available through NCI's caBIG (Cancer Biomedical Informatics Grid). The summary results for similar data on breast and prostate cancer are already freely available to other researchers at this Web site.
NCI leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at http://www.cancer.gov or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).
The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.
Reference: Amundadottir L., et al. Genome-wide association study identifies ABO Blood Group Susceptibility Variants for Pancreatic Cancer. Nature Genetics.
Huddled at the back of her shed, bleating under a magnificent winter coat and tearing cheerfully at a bale of hay, she is possibly the answer to Japan’s chronic national shortage of organ donors: a sheep with a revolutionary secret.
Guided by one of the animal’s lab-coated creators, the visitor’s hand is led to the creature’s underbelly and towards a spot in the middle under eight inches of greasy wool. Lurking there is a spare pancreas.
If the science that put it there can be pushed further forward, Japan may be spared an ethical and practical crisis that has split medical and political opinion.
As the sheep-based chimera organ technology stands at the moment, says the man who is pioneering it, the only viable destination for the pancreas underneath his sheep would be a diabetic chimpanzee.
The organ growing on the sheep was generated from monkey stem cells but the man behind the science, Yutaka Hanazono, believes that the technology could be developed eventually to make sheep into walking organ banks for human livers, hearts, pancreases and skin.
It could happen within a decade, he guesses, perhaps two.
“We have made some very big advances here. There has historically been work on the potential of sheep as producers of human blood, but we are only slowly coming closer to the point where we can harvest sheep for human organs,” Professor Hanazono told The Times.
“We have shown that in vivo (in a living animal) creation of organs is more efficient than making them in vitro (in a test tube) but now we really need to hurry.”
The reason for Professor Hanazono’s sense of urgency — and for the entire organ harvest project being undertaken at the Jichi Medical University — lies many miles away in Tokyo and with a historical peculiarity of the Japanese legal system.
Japan defines death as the point when the heart permanently stops. The concept of brain death — the phase at which organs can most effectively be harvested from donors — does exist, but organs cannot be extracted at that point.
The long-term effect of the legal definition has been striking: organ donation in Japan is virtually nonexistent, forcing many people to travel abroad in search of transplants. In the United States, the rate of organ donors per million people is about 27; in Japan it is under 0.8.
The effect, say pediatricians, has been especially severe for children. The same law that discounts brain death as suitable circumstances for organ donation broadly prevents children under 15 from allowing their organs to be harvested.
To make matters worse, international restrictions on transplant tourism are becoming ever tougher, making Japan’s position even more untenable. To avert disaster, say doctors, Japan either needs the science of synthetic organ generation to advance faster than seems possible, or it needs a complete rethink on the Japanese definition of death.
In response to the impending crisis, and with Professor Hanazono’s sheep still very much at the experimental stage, a series of revisions to the transplant law have been proposed, but the debate has been divisive.
Taro Nakayama, the MP behind the most liberal revision — a change that would allow organs to be harvested from the brain-dead — is a former paediatrician. “Organ tourism is finished and Japan has to change its ways very quickly,” he said.
Gene genies
— In 1997 US scientist Dr Jay Vacanti grew a human ear from cartilage cells on the back of a mouse. He said he believed that it might be possible to grow knee cartilage and even a human liver
— In 2007 two scientists at the University of Nevada created a sheep with 15 per cent human cells as part of research into farming human organs from animals. Human cells were injected into a sheep’s foetus
— Last month Stelios Arcadiou, an Australian artist, unveiled an ear implanted on his arm. He planned to broadcast the sounds it would “hear” on the internet
— Last week Korean scientists said they had cloned beagles that glowed in the dark. Four puppies were created from cells injected with a gene that made them glow red under UV light
Objectives: To determine overall mortality and timing of death in patients with severe acute pancreatitis and factors affecting mortality.
Methods: This was a retrospective, observational study of 110 patients admitted to a general intensive care unit (ICU) from January 2003 to January 2006.
Results: The overall mortality rate was 53.6% (59/110); 25.4% (n = 15) of deaths were early (≤14 days after ICU admission). There were no significant differences in age, sex, or surgical/medical treatment between survivors and nonsurvivors. Median Acute Physiology and Chronic Health Evaluation (APACHE) II score was higher among nonsurvivors than survivors (score = 26 vs 19, respectively; P < 0.001), and the duration of hospitalization before ICU admission was significantly longer (4 vs 1 day; P < 0.001). Among the 59 patients who died, those in the early-mortality group were admitted to the ICU significantly earlier than those in the late-mortality group (3 vs 6.5 days; P < 0.05).
From the *Clinical Center of Serbia, Belgrade, Serbia; †St James's University Hospital, Leeds, UK; and‡Institute for Medical Statistics and Informatics, Belgrade University School of Medicine, Belgrade, Serbia.
Received for publication September 8, 2007; accepted June 25, 2008.
Reprints: Zorica Jankovic, MD, PhD, St James's University Hospital, Beckett Street, Leeds, LS9 7TF, UK (e-mail: Zorica.Jankovic@leedsth.nhs.uk).
This study was supported by the research grant from the Chuongbong Academic Research Fund of the Cheju National University in 2007. Abstract
Objectives: The purpose of this systematic review was to investigate the association between dietary intake of citrus fruits and pancreatic cancer risk.
Methods: Authors searched electronic databases and the reference lists of publications of studies addressing diet and pancreatic cancer up to December 2007. All of the epidemiological studies that obtained individual data on dietary intake of citrus fruits and presented risk estimates of the association between intake of citrus fruits and risk of pancreatic cancer were identified and included. Using general variance-based methods, study-specific odds ratios (ORs)/relative risk and associated confidence interval (CI)/SE for highest versus lowest intake of citrus fruits level were extracted from each article.
Results: Nine articles including 4 case-control studies and 5 cohort studies proved eligible. Overall summary OR using random effect model suggested an inverse association in risk of pancreatic caner with intake of citrus fruits (summary OR, 0.83; 95% CI, 0.70-0.98) with large heterogeneity across studies (I2 = 49.9%).
Bae, Jong-Myon MD, PhD*; Lee, Eun Ja MD, PhD†; Guyatt, Gordon MD, MSc‡
From the *Department of Preventive Medicine, Cheju National University College of Medicine, Jejudo; †Department of Radiology, Myongji Hospital, Kwandong University, College of Medicine, Koyang, Korea; and ‡CLARITY Research Group, Department of Clinical Epidemiology & Biostatistics, Health Sciences Centre, McMaster University, Hamilton, Ontario, Canada.
Received for publication April 15, 2008; accepted July 31, 2008.
Reprints: Jong-Myon Bae, MD, PhD, 1-Ara-1-dong Jeju, Jejudo, 690-756, Republic of Korea (e-mail: jmbae@cheju.ac.kr).
The islet cells within the pancreas are those that are responsible for producing insulin. These are the cells they are hoping to find happy and healthy within Caseys diseased pancreas, and to remove them. Transplanting them into her liver.
(Photo courtesy of T.C. Brelje and R.L. Sorenson).
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 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.
I am excited to hear what this doctor has to say about her pancreas. I believe we may have found a doctor that is not afraid of someone with pancreatitis. (Wouldn't that be 'wunnaful')?!?
That is what I know for today. hehehe
A bit chilly outside- Knowing it is chilly like that outside, makes it hard to disrobe to get in the shower on the inside. (It does too make sense)!
NOTE: Before you read from here, know that I am posting and saving this information for my own benefit; as well as for those of you that might want to know more about Casey's disease, diagnosis and prognosis. Or even for your own info. . . .
. . Good Morning, Having done a million hours of searching online over the past 3 years, it has occurred to me that although I find interesting things about Chronic Pancreatitis, I have yet to find that 'magical' diagnosis/prognosis as it applies to her.
Casey has had two days of excruciating and debilitating pain.
Rough days for her... . .
. . Please pray. *Please do not feel as though you must read this all.
Chronic Pancreatitis is an ongoing inflammation of the pancreas over a prolonged period. Most cases of chronic pancreatitis are caused by alcohol overuse.
Complications of Chronic Pancreatitis are secondary conditions, symptoms, or other disorders that are caused by Chronic Pancreatitis. In many cases the distinction between symptoms of Chronic Pancreatitis and complications of Chronic Pancreatitis is unclear or arbitrary.
Chronic pancreatitis is a painful condition of the pancreas.
Some evidence suggests that chronic pancreatitis may increase the risk of pancreatic cancer.
(Source: excerpt from What You Need To Know About Cancer of the Pancreas: NCI)
********
Treatment (Tx)
I.V. fluid replacement,
morphine,
diazepam,
antibiotics,
calcium gluconate,
insulin
********
The list of complicationsthat have been mentioned in various sources for Chronic Pancreatitis includes:
* Abdominal pain
* Diabetes
* Mild hyperglycemia
* Malabsorption
* Pancreas calcification
* Insulin deficiency
* Glucagon deficiency
* Hypoglycemia unawareness
* IGT (Impaired Glucose Tolerance)
* Diabetes
* Type 1 Diabetes
* Type 2 Diabetes
* Pancreas cyst
* Pancreas abscess
********
Complications and sequelae of Chronic Pancreatitis from the Diseases Database include:
* Diarrhea
* Hyperglycemia
* Back pain
* Parotid gland enlargement
* Pancreatic pseudocyst
* Abdominal pain
* Malabsorption syndrome
********
Obstruction
Gallstone pancreatitis
Choledocholithiasis
Ampullary tumors
Pancreatic tumors
Metastatic carcinoma to pancreas
Periampullary diverticulum
Choledochocele
Choledochal cyst
Duodenal cyst
Pancreatic calculi
Pancreatic duct stricture*
Pancreatic pseudocyst
Pancreatic abscess
Sclerosing cholangitis
Hypertensive sphincter of Oddi
Stenosis or fibrosis of the papilla* ********
Congenital/inherited disorders
Pancreas divisum*
Hereditary pancreatitis*
Cystic fibrosis*
Annular pancreas
Heterotopic pancreas
Duodenal duplication
Alpha1-antitrypsin deficiency*
********
Toxins
Alcohol*
Methanol
Organophosphate insecticides
Scorpion venom
Occupational chemicals
********
Drugs
Azathioprine
6-Mercaptopurine
Thiacide diuretics
Furosemide
Ethacrynic acid
Tetracycline
Sulfonamides
Nitrofurantoin
Metronidazole
Erythromycin
Pentamidine
Didanosine
Sulfasalazine
5-Acetylsalicylic acid products
l-Asparaginase
Oral contraceptives
Corticosteroids
Estrogens
Valproic acid
Methyldopa
Cimetidine
Ranitidine
Sulindac
Acetaminophen
Salicylates
Octreotide
********
Metabolic disorders
Hypertriglyceridemia
Hypercalcemia
Hyperparathyroidism*
******** Trauma
Blunt or penetrating trauma*
Surgical trauma
Endoscopic retrograde cholangiopancreatography
Endoscopic sphincterotomy
Sphincter of Oddi manometry
********
Vascular causes
Postoperative pancreatitis
Atherosclerotic emboli
Cardiopulmonary bypass surgery
Malignant hypertension
Ergotamine overdose
Systemic lupus erythematosus
Polyarteritis nodosa
********
Infections
Bacterial Mycoplasma
Campylobacter jejuni
M. tuberculosis
Legionella
Leptospirosis
M. avium complex
********
Viral
Mumps
Rubella
Hepatitis A, B, C
HIV
CMV
Coxsackievirus B
Epstein-Barr
Adenovirus
Varicella
Echo virus
********
Fungal: Candida albicans infection Aspergillosis
********
Parasitic
Clonorchiasis
Ascariasis
Cryptosporidiosis
Toxoplasmosis
********
Miscellaneous
Penetrating gastrointestinal ulcer
Duodenal Crohn's disease
Protein-calorie malnutrition
Tropical pancreatitis*
Reye's syndrome
Hypothermia
Idiopathic pancreatitis*
Posttransplantation
Food allergy
Chronic renal insufficiency
Severe burns
Long-distance running
Bulimia
Eosinophilic pancreatitis
********
❑ Acute and Chronic pancreatitis is a life-threatening emergency. Provide meticulous supportive care, and continuously monitor the patient.
❑ Monitor the patient vital signs and pulmonary artery pressure closely.
❑ Monitor the patient fluid intake and output and electrolyte levels.
❑ Assess the patient for crackles, rhon-chi, decreased breath sounds, or respiratory failure.
❑ Observe the patient for signs of calcium deficiency, such as tetany, carpopedal spasm, cramps, and seizures.
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CLINICAL TIP: Serum calcium levels decrease in acute pancreatitis, possibly from fat necrosis, resulting in a binding of calcium with free fatty acids.
Muscle twitching,
tremors,
and irritability are signs of decreased calcium levels.
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❑ Administer analgesics, as needed, to relieve the patient’s pain and anxiety.
❑ Observe the patient for adverse reactions to antibiotics: nephrotoxicity with aminoglycosides, pseudomembranous enterocolitis with clindamycin, and blood dyscrasias with chloramphenicol.
❑ Monitor the patient for complications due to total parenteral nutrition, such as sepsis, hypokalemia, overhydration, and metabolic acidosis.
❑ Observe the patient for signs of sepsis, such as fever, cardiac irregularities, changes in arterial blood gas measurements, and deep respirations.
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In the Western Hemisphere, Europe, and Japan the most common cause of chronic calcifying pancreatitis is alcoholism. Other etiologies include idiopathic (up to 40%), biliary tract disease (usually acute rather than chronic), hyperparathyroidism, hereditary pancreatitis, cystic fibrosis, trauma, tropical pancreatitis, and hyperlipidemia. ********
CLINICAL FINDINGS: Chronic pancreatitis can present with mild recurrent bouts of pain, constant abdominal or back pain, or in a small number of patients, painless exocrine and endocrine deficiency. Alcoholism is usually present for 5-10 years prior to the development of clinical pancreatitis. Initially, exocrine function is minimally impaired, but as insufficiency develops, fat and protein malabsorption occur with weight loss. Diabetes occurs in 10% of cases and impaired glucose tolerance in 14-90%. Duodenal obstruction and/or obstructive jaundice may occur in 45% of patients with moderate or advanced chronic pancreatitis. ********
PATHOLOGY: Chronic calcifying pancreatitis is characterized by a nodular, misshapen, hard gland that can be enlarged or shrunken. Calculi are present and are almost always within the ductal system. They vary in size from microscopic concretions to 1-2 cm stones. ********
RADIOLOGY: Demonstration of pancreatic lithiasis on plain films is a fast and inexpensive means of confirming a clinical diagnosis of chronic pancreatitis and effectively excluding carcinoma. In various series the frequency of plain film calcification has varied from 20 to 50% in alcoholic chronic pancreatitis. By contrast, only 2% or less of patients with chronic pancreatitis from biliary disease develop pancreatic calculi.
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SONOGRAPHY: Due to the presence of fibrosis within the gland, there is sometimes sonographic evidence of an inhomogeneously abnormal echo texture often accompanied by calcifications. These calcifications are in the ductal system; their distribution may be focal or diffuse, and if large enough they are associated with acoustical shadowing. The gland is often irregular in outline and there may be enlargement (focal or diffuse) or parenchymal atrophy. Pancreatic ductal dilatation is often visible due to obstructing stones or stricture.
Chronic pancreatitis can be associated with thrombosis of the portal venous system. This usually involves the splenic vein; however, extension to involve the main portal vein can also occur.
Echogenic thrombus may be identified within the involved portion of the vein accompanied by demonstration of collateral channels. In some instances, the obstructed vein itself cannot be sonographically identified.
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CT: The gland in chronic pancreatitis can be normal in size or enlarged or it may be small, atrophic and replaced by fat. When the gland is enlarged, this enlargement may be focal or diffuse. Focal enlargement due to chronic pancreatitis (which is nearly always in the pancreatic head) is hard to distinguish on CT grounds alone from carcinoma unless punctate calcifications are present as these are almost never found in carcinoma (except sometimes following chemotherapy). The incidence of pancreatic carcinoma is low (except for familial pancreatitis) in patients with chronic pancreatitis. The calcifications that are often present in chronic pancreatitis are easily seen on CT (which is the most sensitive modality for their demonstration) and are usually multiple. They may occur in only one part of the gland or be present throughout.
Pancreatic ductal dilatation (greater than 3 mm) is often present, especially when a focal mass with calcification involves the head. The ductal dilatation may be irregular (73%), smooth (15%), or beaded (12%). Common bile duct dilatation may be associated. Occasionally in chronic pancreatitis, CT may show only a markedly dilated beaded pancreatic duct which can simulate a number of small intrapancreatic pseudocysts.
The presence of thrombosis in the portal system can be inferred when a vein fails to opacify normally following intravenous contrast injection and collateral channels are demonstrated.
Patients with chronic pancreatitis can have all the symptoms and signs of pancreatic carcinoma. If a noncalcified focal mass is found in the pancreas of such a patient, then pancreatic carcinoma has to be considered. The presence of the characteristic dense calcifications of chronic pancreatitis within a mass makes it unlikely that it represents a pancreatic cancer. If a diagnostic dilemma exists, then a percutaneous needle aspiration should be considered. ********
False Positives/Negatives
Chronic pancreatitis and pancreatic carcinoma share many CT features, and occasionally, differentiation may be impossible. Obliteration of the fat sleeve around the superior mesenteric artery has been described in both chronic pancreatitis and pancreatic carcinoma.
Pseudotumoral enlargement around focal pancreatitis with extensive fibrous tissue proliferation usually fails to enhance after the administration of contrast material. This characteristic makes the differential diagnosis of pancreatic carcinoma difficult. So tell me, did you get this far?
http://www.emedicine.com/med/TOPIC1721.HTM Pancreatic calcifications, often considered pathognomonic of chronic pancreatitis, are observed in approximately 30% of cases.
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PROGNOSIS
* The prognostic factors associated with chronic pancreatitis are age at diagnosis, smoking, continued use of alcohol, and the presence of liver cirrhosis.
* The overall survival rate is 70% at 10 years and 45% at 20 years. In an international study, 559 deaths occurred among patients with chronic pancreatitis, compared to an expected number of 157, which creates a standard mortality ratio of 3.6 (confidence interval 3.3-3.9). Taking the opposite view, the 10-year mortality rate is 30%, and the 20-year mortality rate is 55%.
* The risk of developing pancreatic cancer is approximately 4% at 20 years. Source: Office of Rare Diseases
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Chronic Pancreatitis is listed as a "rare disease" by the Office of Rare Diseases (ORD) of the National Institutes of Health (NIH). This means that Chronic Pancreatitis, or a subtype of Chronic Pancreatitis, affects less than 200,000 people in the US population.
Background Chronic pancreatitis is commonly defined as a continuing chronic inflammatory process of the pancreas, characterized by irreversible morphological changes. This chronic inflammation can lead to chronic abdominal pain and/or impairment of endocrine and exocrine function of the pancreas. Chronic pancreatitis usually is envisioned as an atrophic fibrotic gland with dilated ducts and calcifications. However, findings on conventional diagnostic studies may be normal in the early stages of chronic pancreatitis, as the inflammatory changes can be seen only by histologic examination.
By definition, chronic pancreatitis is a completely different process from acute pancreatitis. In acute pancreatitis, the patient presents with acute and severe abdominal pain, nausea, and vomiting. The pancreas is acutely inflamed (neutrophils and edema), and the serum levels of pancreatic enzymes (amylase and lipase) are elevated. Full recovery is observed in most patients with acute pancreatitis, whereas in chronic pancreatitis, the primary process is a chronic irreversible inflammation (monocyte and lymphocyte) that leads to fibrosis with calcification. The patient with chronic pancreatitis clinically presents with chronic abdominal pain and normal or mildly elevated pancreatic enzyme levels; when the pancreas lose its endocrine and exocrine function, the patient presents with diabetes mellitus and steatorrhea.
Pathophysiology
Causes of chronic pancreatitis The main causes of chronic pancreatitis include the following:
Alcoholism: Changes appear to develop slowly and may develop after excessive alcohol consumption for 10 years or more. Alcoholism is associated with chronic pancreatitis in 70% of patients.2
Cholelithiasis: Cholelithiasis is a common cause of acute pancreatitis, but it probably is associated with chronic pancreatitis in 20-25% of patients.3
Idiopathic: Etiology is idiopathic in 20% of patients.2
Drug use: Usually, drug-induced pancreatitis is an acute process and does not evolve into a chronic form.
Hereditary causes: Hereditary pancreatitis is an autosomal dominant disorder. Symptoms usually appear in the patient's first decade of life and eventually lead to both exocrine and endocrine pancreatic dysfunction.
Autoimmune disease: Autoimmune pancreatitis is a rare condition that is often seen in patients with primary sclerosing cholangitis.
Congenital causes: A congenital abnormality of fusion, pancreas divisum, can cause chronic pancreatitis
Cystic fibrosis: This disease is associated with pancreatic atrophy and chronic pancreatitis
Other conditions: Hyperlipidemia, hyperparathyroidism, and uremia can cause chronic pancreatitis. Categories of chronic pancreatitis Chronic pancreatitis can be classified into 3 categories: (1) chronic calcifying pancreatitis, (2) chronic obstructive pancreatitis, and (3) chronic inflammatory pancreatitis.
Chronic calcifying pancreatitis
Chronic calcifying pancreatitis is invariably related to alcoholism. The earliest finding is precipitation of proteinaceous material in the pancreatic ducts that forms protein plugs that subsequently calcify. The ducts and lobules are initially involved in a random manner, and they are surrounded by normal parenchymal tissue. However, as the disease progresses, these normal areas become more diffuse. The pancreatic ductal epithelium undergoes atrophy, hyperplasia, and metaplasia at the site of the protein plugs. Many of the small pancreatic ductules dilate, while others are obliterated by fibrosis.
The main pancreatic duct shows a chain-of-lakes appearance due to alternating stenoses and dilatation. In approximately 50% of patients with chronic calcific pancreatitis, the pancreatic parenchyma contains cysts of varying sizes (several millimeters to 5 cm). These cysts are lined by cuboidal epithelium and contain pancreatic enzymes. Peripancreatic fibrosis is usually a late finding that involves the portal and/or splenic veins. Peripancreatic fibrosis causes stenosis or occlusion of retroperitoneal lymph channels. Ascites may complicate chronic calcific pancreatitis as a result of portal hypertension or lymphatic obstruction in 1-2% patients.
Chronic obstructive pancreatitis
In chronic obstructive pancreatitis, the prominent histologic changes are periductal fibrosis and subsequent ductal dilatation. These changes are much more focal than those in the other forms, and in most patients, the changes involve only the portion of the pancreas in which ductal drainage is impaired. Diffuse changes may occur, in which the main pancreatic duct or ampulla is obstructed. Although protein inspissation may occur, histologic changes in the ductal mucosa are less common, and calcification is unusual. Moreover, the pancreatic duct is dilated, and the pancreas is normal in size, atrophic, or focally and/or globally enlarged. A variety of factors are implicated in chronic obstructive pancreatitis; these include ductal obstruction due to ampullary stenosis, inflammatory or neoplastic causes, surgical ductal ligation, and fibrosis due to a pseudocyst as a complication of an episode of acute pancreatitis.
Chronic inflammatory pancreatitis
Chronic inflammatory pancreatitis is rare and can affect elderly persons without a previous history of alcohol excess.
Autoimmune pancreatitis Autoimmune-related chronic pancreatitis is a distinct clinical entity, which may present with signs of acute or chronic pancreatitis, sometimes associated with cholestatic jaundice. On imaging, it may appear as diffuse (duct destructive) or pseudotumoral lesions. These 2 aspects are probably different clinical forms of chronic autoimmune pancreatitis.4
Some autoimmune diseases are associated with chronic autoimmune pancreatitis, but not consistently. One such disease involves a bile disorder that is very similar to primary sclerosing cholangitis but is responsive to corticosteroid treatment. Pancreatitis may be associated with Crohn disease and ulcerative colitis and thus provides justification to investigate patients with idiopathic pancreatitis for underlying inflammatory bowel disease. Chronic autoimmune pancreatitis must always be considered in patients with a pancreatic mass that is atypical for carcinoma on imaging or clinical findings. Corticosteroid therapy for 4 weeks in patients with pancreatic adenocarcinoma is probably less harmful than pancreatectomy (or chemotherapy) in patients with chronic autoimmune pancreatitis.
Diagnosis depends on clinical and radiologic findings. The diagnostic value of serologic markers and, especially, autoantibodies must still be clarified.
Degree of Confidence Currently, CT is regarded as the imaging modality of choice for the initial evaluation of suggested chronic pancreatitis. The diagnostic features of pancreatic enlargement, pancreatic calcifications, pancreatic ductal dilatation, thickening of the peripancreatic fascia, and bile duct involvement are depicted well on CT scans.
CT is more sensitive than plain radiography and ultrasonography in the depiction of pancreatic calcification. Moreover, CT depicts calcification in the pancreas, and confusion with nonpancreatic calcification is less likely. The accuracy of CT is 59-95%; the wide variation is due to the wide discrepancy in the criteria used for diagnosis and in the quality of CT scanners. CT helps in the diagnosis of atrophy of the pancreas, providing better results than ultrasonography.
False Positives/Negatives Chronic pancreatitis and pancreatic carcinoma share many CT features, and occasionally, differentiation may be impossible. Obliteration of the fat sleeve around the superior mesenteric artery has been described in both chronic pancreatitis and pancreatic carcinoma.
Pseudotumoral enlargement around focal pancreatitis with extensive fibrous tissue proliferation usually fails to enhance after the administration of contrast material. This characteristic makes the differential diagnosis of pancreatic carcinoma difficult.
Findings In most patients, a normal pancreatic duct is seen on images obtained with T2-weighted short-tau inversion recovery MRI sequences and MRCP. MRCP may depict the characteristic beaded appearance of the pancreatic duct in chronic pancreatitis. Pancreatic duct calculi are depicted as round filling defects. In chronic pancreatitis, fat-suppressed T1-weighted images usually show a loss of signal intensity. This loss is explained by the fact that pancreatic fibrosis decreases the proteinaceous fluid content of the pancreas, resulting in loss of pancreatic signal intensity. Fibrosis is associated with decreased vascularity, which causes decreased pancreatic gadolinium enhancement.
Small punctate pancreatic calcification is difficult to detect by using MRI, but larger calcifications may be seen as foci of a signal void. As a result of its ability to depict fluid, T2-weighted MRI may demonstrate pancreatic and common bile duct irregularities and pseudocysts associated with chronic pancreatitis.
Parenchymal gadolinium enhancement is a useful technique in evaluating focal areas of inflammation. Compared with normal pancreatic segments, inflamed areas have decreased enhancement in the arterial phase and increased enhancement in the equilibrium phase.
Currently, the diagnosis of early chronic pancreatitis is difficult. With future improvement in spatial resolution and with the use of secretin-enhanced pancreatography, the detection of subtle changes of the side branches may allow the earlier noninvasive diagnosis of chronic pancreatitis. Secretin-enhanced pancreatography also has the potential to depict the anatomic relationships of pancreatic ducts and pseudocysts and to aid in the evaluation of pancreatic exocrine function.
Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with troublemoving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.
Degree of Confidence Because of the introduction of faster imaging sequences and phased-array coils, the accuracy of MRCP has improved considerably, although some concern remains regarding the resolution of smaller pancreatic ducts.
Secretin-enhanced MRCP improves the detection of diseased pancreatic ducts when no abnormality can be shown in physiologic conditions. It also provides additional functional information regarding pancreatic exocrine function. As experience grows, MRI imaging, particularly MRCP, may be increasingly used in assessing and screening for chronic pancreatitis.
False Positives/Negatives Standard good-quality protocols are important with MRCP; otherwise, poor examination technique may create false lesions, which may increase the frequency of unnecessary ERCP examinations.
