A criticalist's view of canine pancreatitis (Proceedings) - Nutritional Management of Pancreatitis in Dogs

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Pancreatitis prednisone dogs



  Recent human case studies have indicated that corticosteroids may even induce acute pancreatitis [21, 22]. In dogs with hyperadrenocorticism. Historically, the use of glucocorticoids has been avoided in dogs with acute pancreatitis. Glucocorticoids are no longer believed to cause. Dogs treated with steroids showed an improved survival and a reduction in the severity of the acinar lesion. Ultrastructurally, pancreatic changes in these. ❿  


- How I Diagnose/How I Treat--Chronic Pancreatitis in Dogs - WSAVA - VIN



  Pankreatitis bei der Katze. In turn, sepsis can contribute to multiple organ failure and decreased survival rates. Biopsy of the pancreas can be used to identify pancreatic cancer. Pulmonary Patterns.     ❾-50%}

 

Pancreatitis prednisone dogs.A criticalist's view of canine pancreatitis (Proceedings)



    It is the development of multi-systemic abnormalities that separates mild from severe, potentially fatal pancreatitis. It is possible that the addition of omega-3 fatty acids, pancreatic enzymes, medium-chain triglycerides, and the amino acid l-glutamine to the liquid nutrition may also help with recovery, though this must be done with caution.

High fat diets and dietary indiscretions are the most common clinically quoted causes of pancreatitis. Yet, there is little scientific evidence for these etiologies. The use of corticosteroids has also been quoted as an underlying cause. Corticosteroid use in dogs causes serum lipase activity to increase.

However, several studies have shown no pancreatic lesions in animals receiving corticosteroids; the lipase must be another type of lipase. However, a lot of patients receiving steroid therapy have diseases that predispose them to pancreatitis, so the primary disease process may be at fault, not the steroids administered to treat those diseases.

Etiologies that have been shown to cause pancreatitis include certain drugs, most commonly potassium bromide, hypercalcemia, hyperlipidemia, especially in miniature Schnauzers, pancreatic hypoperfusion from general anesthesia or hypovolemia, and trauma. Immune-mediated disease, common in the human population with pancreatitis, may play a role in many of the canine patients with pancreatitis, although this has yet to be studied.

Irrespective of the initiating cause, pancreatitis is generally believed to occur when digestive enzymes are activated prematurely within the pancreas. In the normal pancreas, safeguards are present to ensure that harmful pancreatic enzymes are not activated until they reach the intestinal lumen. Enzymes are stored in zymogen granules within the acinar cell in the presence of pancreatic secretory trypsin inhibition and are released at the apical surface directly into the duct system.

They are only activated in the intestine, by trypsin, following the cleavage of trypsinogen by enterokinase.

In clinical pancreatitis, it is thought that inappropriate premature activation of trypsin from trypsinogen in the acinar cells initiates a cascade of early activation of zymogens, especially pro-elastase and pro-phospholipase, leading to auto-digestion of the pancreas.

Often pancreatic inflammation is a self-limiting process, but in some animals reduced pancreatic blood flow and leukocyte and platelet migration into the inflamed pancreas may cause progression to pancreatic necrosis. Secondary infection may arise by bacterial translocation from the intestine or ascending infection up the pancreatic duct.

Release of active pancreatic enzymes and inflammatory mediators from the inflamed pancreas amplifies the severity of pancreatic inflammation, and adversely affects the function of many organs systemic inflammatory response , and cause derangement in fluid, electrolyte and acid-base balance.

It is the development of multi-systemic abnormalities that separates mild from severe, potentially fatal pancreatitis. Histologically, acute pancreatitis is characterized by findings that range from pancreatic edema to necrosis, variable infiltrates of mononuclear and polymorphonuclear cells, and local changes such as peri-pancreatic fat necrosis and thrombosis.

Acute pancreatitis may resolve or persist and can be complicated by secondary infection and pseudocyst or abscess formation. It is tempting to equate mild acute pancreatitis with pancreatic edema, and severe or fatal pancreatitis with pancreatic necrosis, but this relationship has not been critically examined in patients with naturally occurring pancreatitis.

Pancreatitis tends to occur in middle-aged, neutered dogs with no gender preference. Dogs with pancreatitis are often overweight. Terrier and non-sporting breeds tend to be overrepresented. As noted earlier, presenting signs are often non-specific and can include vomiting, diarrhea, anorexia, and abdominal pain.

Examination findings are also non-specific for many abdominal disorders and can include fever or hypothermia, tachycardia, tachypnea, evidence of decreased perfusion such as pale mucus membranes and hyper- or hypodynamic pulses, evidence of dehydration such as tacky or dry mucus membranes and prolonged skin turgor, absent intestinal borborygmi, abdominal pain, abdominal distention due to ascites, and icterus.

However, amylase and lipase have been shown to be produced by multiple organs and their elimination can be affected by other organ dysfunction, making elevation of these enzymes non-specific for the diagnosis of pancreatitis. Abdominal radiographs may or may not have findings that are suggestive of pancreatitis, even in the presence of known pancreatitis.

Abdominal ultrasound was, and remains, a standard test for diagnosing acute pancreatitis. Abdominal ultrasonography often finds abnormalities that suggest or are consistent with pancreatitis as well as eliminate other potential causes of vomiting and abdominal pain. One may sometimes detect hypoechogenicity of the pancreas surrounded by hyperechoic fat in the region of the pancreas that is due to pancreatitis.

At other times, a markedly thickened pancreas may be found. Ultrasonography currently seems to be the fastest test with reasonably "good" sensitivity and specificity for pancreatitis in the dog.

However, ultrasonography is not perfect: it is very operator dependent, and false positive and false negative results are possible, even in the hands of an experienced operator. A test for trypsin-like immune-reactivity TLI was developed. This test was found to be diagnostic for pancreatic insufficiency, but several issues with the test as a diagnostic for pancreatitis were noted: renal failure can falsely elevated TLI values and a normal TLI value does not exclude acute pancreatitis as a diagnosis.

More recently, several tests to measure pancreatic lipase immuno-reactivity have been developed. These tests evaluate the serum for the specific lipase produced and released by the pancreas. Because of the short half-life of pancreas-specific lipase 90 minutes , continuous secretion of high levels of this enzyme into the circulation is needed for a diagnosis of pancreatitis.

A tube can be placed into the jejunum part of the small intestine if needed to provide enteral nutrition when vomiting cannot be controlled. Chronic pancreatitis refers to a continuing, smoldering, low-grade inflammation of the pancreas. Symptoms such as vomiting and discomfort after eating may occur intermittently, sometimes accompanied by depression, loss of appetite, and weight loss.

In some cases, signs may be as subtle and nonspecific as a dog not wanting to play normally, being a picky eater, or skipping a meal from time to time. Chronic pancreatitis may periodically flare up, resulting in acute pancreatitis. Dogs with chronic pancreatitis often respond favorably to a low-fat diet. Pain medication can be helpful in relieving the symptoms of chronic pancreatitis and may speed recovery.

Chronic pancreatitis is often subclinical and may be more common than is generally realized, with symptoms blamed on other diseases.

It may also occur concurrently with conditions such as IBD inflammatory bowel disease and diabetes mellitus. In addition to digestive enzymes exocrine function , the pancreas also produces insulin endocrine function.

Dogs who are diabetic may have an increased risk for pancreatitis. Conversely, a dog whose pancreas is damaged due to pancreatitis may develop diabetes, which can be either temporary or permanent; 30 percent of diabetes in dogs may be due to damage from chronic pancreatitis.

Exocrine pancreatic insufficiency EPI , when the pancreas is no longer able to produce digestive enzymes, can also result from chronic pancreatitis, leading to weight loss despite consuming large amounts of food. When the pancreas is damaged, diabetes is likely to show up several months before EPI. Pancreatitis is often blamed on high-fat diets, though there is little scientific evidence to support this. Active, working dogs, such as sled dogs, can eat as much as 60 percent fat in their diets without developing pancreatitis, but too much fat may cause trouble for middle-aged, overweight, relatively inactive dogs, who are the ones most commonly affected by pancreatitis.

Too much fat can also cause problems for some dogs with chronic pancreatitis. Dietary indiscretion, such as eating rancid fatty scraps from the garbage, can also lead to pancreatitis, particularly when a dog accustomed to a low- or normal-fat diet ingests high-fat foods.

Low-protein diets have also been shown to predispose dogs to pancreatitis, especially when combined with high fat intake. Some prescription diets may be a concern, such as those prescribed to dissolve struvite bladder stones; to prevent calcium oxalate, urate, or cystine stones; and to treat kidney disease; especially for breeds prone to pancreatitis. Several medications have been associated with pancreatitis, most recently the combination of potassium bromide and phenobarbital used to control epilepsy.

This combination has a much higher risk of causing pancreatitis than phenobarbital alone no studies have been done on the use of potassium bromide by itself. Many other medications have been linked to pancreatitis, though the relationship is not always clear. These include certain antibiotics sulfa drugs, tetracycline, metronidazole, nitrofurantoin ; chemotherapy agents azathioprine, L-asparaginase, vinca alkaloids ; diuretics thiazides, furosemide ; other antiepileptic drugs valproic acid, carbamazepine ; hormones estrogen ; long-acting antacids cimetidine, ranitidine ; Tylenol acetaminophen ; and aspirin salicylates.

Corticosteroids, such as prednisone, are especially controversial: while veterinarians have long considered them to be the most common drug to cause pancreatitis, recent human studies have discounted this link.

Based on anecdotal evidence, however, I believe the association does exist in dogs. I personally know dogs who developed pancreatitis within days of being given corticosteroids. Toxins, particularly organophosphates insecticides used in some flea control products , as well as scorpion stings and toxic levels of zinc, may also lead to pancreatitis.

Certain conditions may predispose a dog to pancreatitis. Both diabetes and hypothyroidism can affect fat metabolism and lead to hyperlipidemia, which may predispose a dog to pancreatitis. Miniature Schnauzers are prone to developing hyperlipidemia and thus may have an increased risk of pancreatitis. Obesity predisposes dogs to pancreatitis, and the disease is often more severe in dogs who are overweight. Pancreatitis can occur in dogs of any age, breed, or sex.

That said, most dogs with pancreatitis are middle-aged or older, overweight, and relatively inactive. Cavalier King Charles Spaniels, Collies, and Boxers have been shown to have an increased relative risk of chronic pancreatitis, and Cocker Spaniels an increased relative risk of acute and chronic pancreatitis combined. Dachshunds have been reported to be predisposed to acute pancreatitis.

Other breeds mentioned as having an increased risk for pancreatitis include the Briard, Shetland Sheepdog, Miniature Poodle, German Shepherd Dog, terriers especially Yorkies and Silkies , and other non-sporting breeds. Humans sometimes develop autoimmune chronic pancreatitis, and it is theorized that dogs may as well. German Shepherd Dogs have been shown to develop immune-mediated lymphocytic pancreatitis, which predisposes them to pancreatic atrophy.

Pancreatitis has been associated with immune-mediated diseases, which may include IBD, though the cause-and-effect relationship is not understood. While there is no scientific evidence to support this, some doctors have suggested that food allergies could be a rare cause of recurrent or chronic pancreatitis.

I think IBD could possibly be both a cause and an effect of pancreatitis, or that both could be caused by an underlying autoimmune disease or food allergy. Dogs with immune-mediated pancreatitis may respond well to corticosteroids such as prednisone, which suppress the immune system, even though this drug has also been thought to cause acute pancreatitis. Trauma to the pancreas, such as a result of the dog being hit by a car, can lead to inflammation and pancreatitis.

Surgery has also been linked to pancreatitis, probably due to low blood pressure or low blood volume caused by anesthesia.

Gallstones choleliths can block the bile duct, and thus the flow of digestive enzymes from the pancreas and can lead to pancreatitis in people; it is likely that the same would be true for both species pancreatitis can also block the flow of bile from the gall bladder. Other theoretical causes include bacterial or viral infections; vaccinations; obstruction of the pancreatic duct; reflux of intestinal contents up the pancreatic duct; impaired blood supply to the pancreas due to shock, gastric-dilatation volvulus bloat , or other causes; and hereditary factors.

In rare cases, pancreatitis can be caused by a tumor in the pancreas. In most cases with dogs, the cause is never found. In humans, pancreatitis is most commonly caused by alcohol abuse. Some blood test results are suggestive of pancreatitis, but not definitive. Substantially elevated three to five times the normal level lipase and amylase, in particular, are strongly supportive of a diagnosis of pancreatitis, but the absence of these signs does not rule it out; lipase and amylase may be normal in as many as half of all dogs with pancreatitis.

With chronic pancreatitis, blood tests are often completely normal, and may be so with acute pancreatitis as well, particularly if it is not severe enough to cause complications.

There are three types of lipase: pancreatic, hepatic, and gastric. Standard blood tests cannot differentiate between them, but the Spec cPL measures only pancreatic lipase. Spec cPL is now considered the best choice for quick and accurate diagnosis, with results available in 12 to 24 hours.

The cPLI test is equally accurate, but not as readily available and the results take longer. In comparison, the cPLI test has 82 percent sensitivity and 98 percent specificity. The Spec cPL test can be repeated every two or three days to help judge response to therapy, and after returning home, to confirm recovery. It can also be used to monitor response to changes in diet and other treatment for dogs with chronic pancreatitis. The Spec cPL test is recommended for any dog whose symptoms include vomiting, anorexia, or abdominal pain.

It can also be used to monitor dogs with chronic pancreatitis, or those with conditions or whose medications predispose them to pancreatitis. In the future, this test may be done as part of standard blood work on normal, seemingly healthy dogs, to identify chronic pancreatitis that may be subclinical not causing recognizable symptoms.

Radiographs detect only 24 to 33 percent of cases of acute pancreatitis, but are also used to identify other causes of vomiting and anorexia, such as intestinal obstruction. An experienced ultrasound practitioner can detect two-thirds of acute pancreatitis cases. Ultrasound may also be used to look for signs of peritonitis, pancreatic abscess or cyst, and biliary obstruction. Neither x-rays nor ultrasound can identify chronic pancreatitis. Biopsy of the pancreas can be used to identify pancreatic cancer.

J Small Anim Pract ;51 1 The anti-inflammatory action of maropitant in a mouse model in acute pancreatitis. J Vet Med Sci ;80 3 Comparative efficacy of maropitant and selected drugs in preventing emesis induced by centrally or peripherally acting emetogens in dogs. J Vet Pharmacol Ther ;31 6 Substance P mediates inflammatory oedema in acute pancreatitis via activation of the neurokinin-1 receptor in rats and mice.

Br J Pharmacol ; 3 ACVIM consensus statement: support for rational administration of gastrointestinal protectants to dogs and cats. J Vet Intern Med ;32 6 Repeated famotidine administration results in a diminished effect on intragastric pH in dogs. J Vet Intern Med ;31 1 Efficacy of oral famotidine and 2 omeprazole formulations for the control of intragastric pH in dogs. J Vet Intern Med ;25 1 Efficacy of intravenous administration of combined acid suppressants in healthy dogs.

J Vet Intern Med ;29 2 Fluid resuscitation in acute pancreatitis. Clin Gastroenterol Hepatol ;6 10 Splanchnic tissue perfusion in acute experimental pancreatitis. Scand J Gastroenterol ;34 3 Pancreatic response to crystalloid resuscitation in experimental pancreatitis. J Surg Res ; Controversies in the use of hydroxyethyl starch solutions in small animal emergency and critical care.

Acta Anaesthesiol Scand ;59 3 Wong C, Koenig A. The colloid controversy: are colloids bad and what are the options? Evaluation of fresh frozen plasma administration in dogs with pancreatitis: 77 cases Comparison of initial treatment with and without corticosteroids for suspected acute pancreatitis in dogs.

J Small Anim Pract ;60 5 Acute pancreatitis in dogs: a review article. EJCAP ; Characteristics and outcomes in surgical management of severe acute pancreatitis: 37 dogs Coleman M, Robson M. Pancreatic masses following pancreatitis: pancreatic pseudocysts, necrosis, and abscesses. Internal Medicine Cases 2. Internal Medicine Cases. Anesthetic Problems. Anesthetic Monitoring. Point-Of-Care Diagnostics. Airway Obstruction. Chronic Pancreatitis. Brachycephalic Syndrome.

Cardiac Arrhythmias. Hepatic Lipidosis. Reptile Pain. Bleeding Animal. Small Intestinal Dysbacteriosis. Adverse Reaction. Recurrent Staphylococcal Infections. Ringworm in Cats. Ventral Spinal Cord Compression. Congenital Abnormalities. Dystocia, Cesarean Section. Medical Treatment, Fluid Therapy. Intervertebral Disc Disease. Cerebellocortical Degeneration. Degenerative Myelopathy. Meningioma Surgery. Seizures in Cats. Seizures in Dogs. COX-2 Therapy. Radiation Therapy.

Mast Cell Tumours. Modern Molecular Therapies. Management of Carcinomas. Lid Diseases. Fundoscopic Exam. Corneal Disorders. Third Eyelid. Corneal Ulcers. Tarsus Conditions. Joint Diseases in Cats. Cranial Cruciate Ligament. Total Hip Replacement. Osteoarthritis Symposium. Behavioral Manifestations.

Critical Care. Dental Diseases. Calcium Metabolism. Gastrointestinal Stasis. Dermatological Problems.

Should you:. The answer is C: Take him to your vet right away. These can be signs of pancreatitis. When signs of abdominal pain accompany vomiting, pancreatitis is high on the list of possible causes. The worst thing you can do is feed your dog fatty food at this time. Pancreatitis literally means inflammation of the pancreas, the glandular organ that secretes enzymes needed to digest food.

When something causes these enzymes to be activated prematurely, they can actually begin to digest the pancreas itself, resulting in pain and inflammation. Pancreatitis occurs in two different forms, acute and chronic, and both may be either mild or severe. Acute pancreatitis occurs suddenly and is more often severe, while chronic pancreatitis refers to an ongoing inflammation that is usually less severe and may even be subclinical no recognizable symptoms.

Acute pancreatitis can be extremely painful, and can become life-threatening if the inflammation spreads, affecting multiple organs and systems. Symptoms commonly include anorexia loss of appetitevomiting, weakness, depression, and abdominal pain. Additional symptoms may include diarrhea, drooling, fever, and collapse. For mild cases, all that may be needed is to withhold food and water for 24 to 48 hours no longeralong with administering IV fluids to prevent dehydration and drugs to stop vomiting and control pain.

For moderate to severe cases, hospitalization and intensive treatment and monitoring is required. Supportive treatment includes intravenous fluids to keep the dog hydrated and restore electrolyte and acid-base balance. Potent pain medication is needed, such as injectable buprenorphine or other narcotic pain relievers. Treatment is generally required for three to five days, and sometimes longer.

Surgery may be necessary, particularly if the pancreas is abscessed or the pancreatic duct is blocked. Recommended medications that stop vomiting antiemetics in dogs with pancreatitis include a metoclopramide infusion and chlorpromazine once dehydration has been controlled. Alternatively, dolasetron Anzemet and ondansetron Zofran — antiemetics developed to combat vomiting that has been induced by chemotherapy — may be used. Cerenia maropitant is a new antiemetic drug approved for dogs that some vets are starting to use, though it has a limited track record.

Metoclopramide Reglana commonly used antiemetic, may be contraindicated in pancreatitis due to concern that it may decrease blood flow to the pancreas antidopaminergic effectthough this has not been substantiated.

Antibiotics to control infections secondary to pancreatitis may be used, though this complication is not thought to be common in dogs. A plasma transfusion is sometimes given in moderate to severe cases in the hopes that it will inhibit active pancreatic enzymes and systemic inflammatory response; it also provides clotting factors that can help prevent and treat disseminated intravascular coagulation DICan often lethal potential side effect of pancreatitis.

Antacids have not been shown to have any beneficial effect in the treatment of pancreatitis, though they may be given when vomiting is persistent or severe. Non-steroidal anti-inflammatory drugs NSAIDs are not effective and should be avoided due to concerns for gastric ulceration and kidney and liver damage.

There are no studies yet to support the use of corticosteroids for treating pancreatitis in dogs. Traditionally, the standard recommendation has been to withhold all oral food and water until symptoms subside, in order to allow the pancreas to rest. If symptoms persisted for more than hours, nutrition was given parenterally intravenously, avoiding the stomach and intestines.

It was thought that even the sight or smell of food could trigger pancreatic secretions that would make the problem worse. Today, though, there is growing evidence in both humans and animals that recovery time is reduced and survival rates increased when patients are fed early in the recovery from pancreatitis. In turn, sepsis can contribute to multiple organ failure and decreased survival rates. Without oral nutrition, the intestines starve, even if nutrition is provided to the rest of the body through IVs.

This is because the intestines receive their nutrition only from what passes through them. Enteral feeding, in which nutrition is provided through the digestive system, is thought to decrease the potential for bacterial infection caused by intestinal permeation, and may reduce the time the dog needs to be hospitalized.

Because most dogs with pancreatitis are unwilling to eat, a liquid diet may be fed via a tube placed through the nose, esophagus, or stomach. Dogs may tolerate nasoesophageal feeding even when vomiting persists. There is evidence that pancreatic secretions are suppressed during an attack of pancreatitis, so food delivered in this manner stimulates the pancreas less than we used to believe, and helps to maintain the health of the gastrointestinal tract and decrease inflammation and side effects such as those listed above.

The ideal composition of this diet has not yet been determined. It is possible that the addition of omega-3 fatty acids, pancreatic enzymes, medium-chain triglycerides, and the amino acid l-glutamine to the liquid nutrition may also help with recovery, though this must be done with caution. Probiotics, however, are not recommended; a recent human study showed an increased death rate for patients with severe acute pancreatitis when probiotics were administered, possibly due to reduced blood flow to the small intestine.

Enteral tube or oral feeding should begin after 48 hours without food. Vomiting can be controlled with antiemetics and pain medication. The goal of nutrition in the short term is to improve barrier function stop leaky gut syndrome rather than to supply total caloric needs. Parenteral IV nutrition should be used only when absolutely necessary, due to persistent, uncontrolled vomiting.

Survival rates improve when it is combined with enteral nutrition. A tube can be placed into the jejunum part of the small intestine if needed to provide enteral nutrition when vomiting cannot be controlled. Chronic pancreatitis refers to a continuing, smoldering, low-grade inflammation of the pancreas. Symptoms such as vomiting and discomfort after eating may occur intermittently, sometimes accompanied by depression, loss of appetite, and weight loss.

In some cases, signs may be as subtle and nonspecific as a dog not wanting to play normally, being a picky eater, or skipping a meal from time to time. Chronic pancreatitis may periodically flare up, resulting in acute pancreatitis. Dogs with chronic pancreatitis often respond favorably to a low-fat diet. Pain medication can be helpful in relieving the symptoms of chronic pancreatitis and may speed recovery. Chronic pancreatitis is often subclinical and may be more common than is generally realized, with symptoms blamed on other diseases.

It may also occur concurrently with conditions such as IBD inflammatory bowel disease and diabetes mellitus. In addition to digestive enzymes exocrine functionthe pancreas also produces insulin endocrine function. Dogs who are diabetic may have an increased risk for pancreatitis. Conversely, a dog whose pancreas is damaged due to pancreatitis may develop diabetes, which can be either temporary or permanent; 30 percent of diabetes in dogs may be due to damage from chronic pancreatitis. Exocrine pancreatic insufficiency EPIwhen the pancreas is no longer able to produce digestive enzymes, can also result from chronic pancreatitis, leading to weight loss despite consuming large amounts of food.

When the pancreas is damaged, diabetes is likely to show up several months before EPI. Pancreatitis is often blamed on high-fat diets, though there is little scientific evidence to support this. Active, working dogs, such as sled dogs, can eat as much as 60 percent fat in their diets without developing pancreatitis, but too much fat may cause trouble for middle-aged, overweight, relatively inactive dogs, who are the ones most commonly affected by pancreatitis.

Too much fat can also cause problems for some dogs with chronic pancreatitis. Dietary indiscretion, such as eating rancid fatty scraps from the garbage, can also lead to pancreatitis, particularly when a dog accustomed to a low- or normal-fat diet ingests high-fat foods. Low-protein diets have also been shown to predispose dogs to pancreatitis, especially when combined with high fat intake.

Some prescription diets may be a concern, such as those prescribed to dissolve struvite bladder stones; to prevent calcium oxalate, urate, or cystine stones; and to treat kidney disease; especially for breeds prone to pancreatitis. Several medications have been associated with pancreatitis, most recently the combination of potassium bromide and phenobarbital used to control epilepsy. This combination has a much higher risk of causing pancreatitis than phenobarbital alone no studies have been done on the use of potassium bromide by itself.

Many other medications have been linked to pancreatitis, though the relationship is not always clear. These include certain antibiotics sulfa drugs, tetracycline, metronidazole, nitrofurantoin ; chemotherapy agents azathioprine, L-asparaginase, vinca alkaloids ; diuretics thiazides, furosemide ; other antiepileptic drugs valproic acid, carbamazepine ; hormones estrogen ; long-acting antacids cimetidine, ranitidine ; Tylenol acetaminophen ; and aspirin salicylates.

Corticosteroids, such as prednisone, are especially controversial: while veterinarians have long considered them to be the most common drug to cause pancreatitis, recent human studies have discounted this link. Based on anecdotal evidence, however, I believe the association does exist in dogs. I personally know dogs who developed pancreatitis within days of being given corticosteroids.

Toxins, particularly organophosphates insecticides used in some flea control productsas well as scorpion stings and toxic levels of zinc, may also lead to pancreatitis. Certain conditions may predispose a dog to pancreatitis.

Both diabetes and hypothyroidism can affect fat metabolism and lead to hyperlipidemia, which may predispose a dog to pancreatitis. Miniature Schnauzers are prone to developing hyperlipidemia and thus may have an increased risk of pancreatitis. Obesity predisposes dogs to pancreatitis, and the disease is often more severe in dogs who are overweight.

Pancreatitis can occur in dogs of any age, breed, or sex. That said, most dogs with pancreatitis are middle-aged or older, overweight, and relatively inactive. Cavalier King Charles Spaniels, Collies, and Boxers have been shown to have an increased relative risk of chronic pancreatitis, and Cocker Spaniels an increased relative risk of acute and chronic pancreatitis combined.

Dachshunds have been reported to be predisposed to acute pancreatitis. Other breeds mentioned as having an increased risk for pancreatitis include the Briard, Shetland Sheepdog, Miniature Poodle, German Shepherd Dog, terriers especially Yorkies and Silkiesand other non-sporting breeds.

Humans sometimes develop autoimmune chronic pancreatitis, and it is theorized that dogs may as well. German Shepherd Dogs have been shown to develop immune-mediated lymphocytic pancreatitis, which predisposes them to pancreatic atrophy. Pancreatitis has been associated with immune-mediated diseases, which may include IBD, though the cause-and-effect relationship is not understood.

While there is no scientific evidence to support this, some doctors have suggested that food allergies could be a rare cause of recurrent or chronic pancreatitis. I think IBD could possibly be both a cause and an effect of pancreatitis, or that both could be caused by an underlying autoimmune disease or food allergy.

Dogs with immune-mediated pancreatitis may respond well to corticosteroids such as prednisone, which suppress the immune system, even though this drug has also been thought to cause acute pancreatitis. Trauma to the pancreas, such as a result of the dog being hit by a car, can lead to inflammation and pancreatitis.

Surgery has also been linked to pancreatitis, probably due to low blood pressure or low blood volume caused by anesthesia. Gallstones choleliths can block the bile duct, and thus the flow of digestive enzymes from the pancreas and can lead to pancreatitis in people; it is likely that the same would be true for both species pancreatitis can also block the flow of bile from the gall bladder. Other theoretical causes include bacterial or viral infections; vaccinations; obstruction of the pancreatic duct; reflux of intestinal contents up the pancreatic duct; impaired blood supply to the pancreas due to shock, gastric-dilatation volvulus bloator other causes; and hereditary factors.

In rare cases, pancreatitis can be caused by a tumor in the pancreas. In most cases with dogs, the cause is never found. In humans, pancreatitis is most commonly caused by alcohol abuse. Some blood test results are suggestive of pancreatitis, but not definitive. Substantially elevated three to five times the normal level lipase and amylase, in particular, are strongly supportive of a diagnosis of pancreatitis, but the absence of these signs does not rule it out; lipase and amylase may be normal in as many as half of all dogs with pancreatitis.

With chronic pancreatitis, blood tests are often completely normal, and may be so with acute pancreatitis as well, particularly if it is not severe enough to cause complications.

The objective of this study was to examine the effects of immunosuppressive prednisolone therapy on pancreatic tissue and the concentration of serum canine. Recent human case studies have indicated that corticosteroids may even induce acute pancreatitis [21, 22]. In dogs with hyperadrenocorticism. Historically, the use of glucocorticoids has been avoided in dogs with acute pancreatitis. Glucocorticoids are no longer believed to cause. Dogs treated with steroids showed an improved survival and a reduction in the severity of the acinar lesion. Ultrastructurally, pancreatic changes in these. In dogs with acute pancreatitis, initial treatment with prednisolone resulted in earlier reductions in C-reactive protein concentration and earlier. Dogs with pancreatitis are often overweight. Interpretation der Lungenmuster. Materials and methods: Sixty-five dogs were included in this non-blinded, non-randomised clinical study. Canine Leptospirosis 1. Healing the digestive tract L-glutamine is an amino acid that can help the intestinal mucosa to recover from the effects of going without food.

Historically, canine pancreatitis was believed to be acute in the majority of cases. However, in a large necropsy study conducted at the Animal Medical Center in New York, histopathologic evidence of chronic pancreatic inflammation was observed almost twice as frequently as was evidence of acute pancreatic inflammation. Chronic pancreatitis should be considered as a potential differential diagnosis in any dog with chronic gastrointestinal signs, where an underlying cause cannot be readily identified.

A careful history should be taken and a thorough physical examination should be completed. Then the patient should be evaluated for endoparasites by a routine fecal smear, fecal flotation, and a therapeutic trial with a broad-spectrum anthelminthic agent. Next, the patient should be evaluated for secondary causes of gastrointestinal disease by performing a complete blood count, a serum chemistry profile, and a urinalysis. Many different cell types in the body synthesize and secrete lipases.

In contrast to catalytic assays for the measurement of lipase activity, use of immunoassays does allow for the specific measurement of lipase originated from the exocrine pancreas. Serum cPLI was measured in a group of dogs with exocrine pancreatic insufficiency and the median serum cPLI concentration was significantly decreased compared to clinically healthy dogs.

In addition, serum cPLI concentration was non-detectable in most of the dogs and minimal serum cPLI concentrations were observed in the rest of the dogs, indicating that serum cPLI concentration originates from the exocrine pancreas and is specific for exocrine pancreatic function. In another study serum cPLI was evaluated in dogs with experimentally induced chronic renal failure. While serum cPLI was significantly higher in dogs with experimentally induced chronic renal failure than in clinically healthy dogs, most dogs had serum cPLI concentrations within the reference range and none of the dogs had serum cPLI concentrations that were above the currently recommended cut-off value for pancreatitis.

These data would suggest that serum cPLI concentration can be used as a diagnostic test for pancreatitis even in dogs with renal failure. Also, long-term oral administration of prednisone did not have any effect on serum cPLI concentration.

Finally, the sensitivity of different minimally-invasive diagnostic tests was compared in dogs with biopsy-proven pancreatitis. Often canine patients with chronic pancreatitis have concurrent conditions, most notably IBD. Very little is known about appropriate therapy for these patients and management is often limited to evaluation and treatment of the concurrent condition, and careful monitoring of the pancreatitis.

Serum calcium and triglyceride concentrations should always be evaluated in these patients in order to identify any risk factors that can potentially be addressed therapeutically. Also, the use of an ultra low-fat diet is recommended in these patients. Patients should be monitored for a decrease in serum cPLI concentration, initially every weeks and less frequently as the condition improves. Over the last two decades a new form of pancreatitis, autoimmune pancreatitis, has been described in humans.

Like many cases of chronic pancreatitis in dogs, autoimmune pancreatitis is characterized by a lymphocytic-plasmacytic infiltration of the pancreas. Sensitivity of serum markers for pancreatitis in dogs with macroscopic evidence of pancreatitis. Vet Ther ; ;. Serum canine pancreatic lipase immunoreactivity cPLI concentrations in dogs with spontaneous pancreatitis. Localization of pancreatic inflammation and necrosis in dogs. J Vet Int Med ; ;. Autoimmune pancreatitis: Clinical and radiological features and objective response to steroid therapy in a UK Series.

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Resuscitation Trends. DIC in GDV Patient. Nutrition Basics. GDV Dog. Antithrombotic Therapy. Canine Hypothyroidism. Feline Diabetes Mellitus. Islet Inflammation. Primary Hyperaldosteronism. Canine Polyuria. MRS Infections. Nosocomial Infections. Antimicrobial Resistance. Antimicrobial Usage. Feline Pancreatitis. Adverse Food Reactions. Canine IBD. Gastrointestinal Disorders. Laboratory Tests. Protein-Losing Enteropathies.

Risk Factors. Breed Related Diseases. Transfusion Medicine. Immune-mediated Hemolytic Anemia. Chronic Hepatitis. Hepatobiliary Diseases. Inflammatory Liver Disease. Human-Animal Interactions. Dog Bite Prevention. Dog Bite Injuries. Infectious Diseases. Canine Leishmaniasis. Feline Leukaemia Virus. Feline Infectious Diseases.

Hemotropic Mycoplasmas. Internal Medicine. Internal Medicine Cases 2. Internal Medicine Cases. Anesthetic Problems. Anesthetic Monitoring. Point-Of-Care Diagnostics. Airway Obstruction. Chronic Pancreatitis.



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