- 0.1 1. Compare acute and chronic pancreatitis.
- 0.2 2. Describe the pathophysiology of severe pancreatitis.
- 0.3 3. What is the most common cause of acute pancreatitis?
- 0.4 4. Why is ingestion of a meal high in fat implicated as a cause of acute pancreatitis in dogs?
- 0.5 5. What are the primary presenting complaints and physical findings in dogs with pancreatitis?
- 0.6 6. Do cats present with the same symptoms as dogs?
- 0.7 7. What are the radiographic signs of pancreatitis?
- 0.8 8. Describe the ultrasonic changes associated with pancreatitis.
- 0.9 9. Are elevations in serum amylase and lipase activities definitive for the diagnosis of pancreatitis?
- 0.10 10. Do normal lipase and amylase values eliminate the possibility of pancreatitis?
- 0.11 11. How is the diagnosis of pancreatitis confirmed?
- 0.12 12. How can the severity of acute pancreatitis be ascertained?
- 0.13 13. What are the key components in treatment of pancreatitis?
- 0.14 14. How is fresh frozen plasma useful in the treatment of pancreatitis?
- 0.15 15. Is there evidence supporting the use of antibiotics or nonsteroidal antiinflammatory agents in pancreatitis?
- 0.16 16. What is the role of surgery in acute pancreatitis?
- 0.17 17. What is done when the patient vomits every time food is offered?
- 0.18 18. What are the long-term complications of pancreatitis?
- 1 Controversies
- 1.1 19. Do corticosteroids cause severe pancreatitis?
- 1.2 20. Should food and water be withheld to allow the pancreas to rest and recover from the inflammatory episode?
- 1.3 21. Should total parenteral nutrition (TPN) be used in the treatment of pancreatitis?
- 1.4 22. Should total enteral nutrition (TEN) be used in the treatment of pancreatitis?
1. Compare acute and chronic pancreatitis.
|Acute inflammatory condition||Long-standing inflammation|
|No evidence of fibrosis||Fibrosis and loss of acinar cell mass|
|Mild or severe||Mild or severe|
|Reversible histopathologic changes||Irreversible histopathologic changes|
2. Describe the pathophysiology of severe pancreatitis.
Severe pancreatitis is characterized by extensive pancreatic necrosis and multiple organ involvement (perhaps even organ failure). The exocrine pancreas produces a number of digestive enzymes necessary for the degradation of proteins, fats, and polysaccharides. These enzymes are synthesized in inactive proenzyme forms that are activated only after they are secreted into the small intestine. In pancreatitis digestive enzymes are activated in the pancreas rather than the intestine because of damage to the gland or some stimulatory signal that results in pancreatic autodigestion. Systemic complications develop as activated pancreatic enzymes enter the bloodstream.
3. What is the most common cause of acute pancreatitis?
In most cases, the cause remains unknown. Causes that are often listed include nutrition (high fat meal), drugs (cholinesterase inhibitors and cholinergic agonists, thiazide diuretics, furosemide, estrogens, azathioprine, L-asparaginase, sulfonamides, tetracycline, metronidazole, cimetidine, ranitidine, acetaminophen, procainamide, and nitrofurantoin), organophosphates, trauma, hypoperfusion, hypercalcemia, hyperlipidemia (Schnauzers), and neoplastic infiltration by pancreatic adenocarcinoma. In cats, pancreatitis also is associated with concurrent hepatic lipidosis, infection with Toxoplasma gondii, and biliary tract inflammation.
4. Why is ingestion of a meal high in fat implicated as a cause of acute pancreatitis in dogs?
The pancreatic enzyme lipase metabolizes ingested triglycerides to free fatty acids in pancreatic capillaries. These fatty acids are directly injurious to the pancreas. The high incidence of pancreatitis in miniature Schnauzers also may be related to the high prevalence of familial hyperlipoproteinemia.
5. What are the primary presenting complaints and physical findings in dogs with pancreatitis?
Common clinical findings are vomiting, abdominal pain, dehydration, and fever. In dogs the duration of vomiting may be several days or, in acute hemorrhagic pancreatitis, only a few hours. Uncommon systemic complications include icterus, respiratory distress, and bleeding disorders.
6. Do cats present with the same symptoms as dogs?
Of interest, whereas vomiting is a common historical finding in dogs, most cats present with anorexia (97%), lethargy (100%), dehydration (92%), hypothermia (68%), vomiting (35%), abdominal pain (25%), a palpable abdominal mass (23%), respiratory distress (20%), ataxia (15%), and diarrhea (15%).
7. What are the radiographic signs of pancreatitis?
The most common radiographic finding is loss of visceral detail (ground-glass appearance) in the right cranial abdomen. Other radiographic signs include displacement of the descending duodenum to the right and of the stomach to the left, presence of a mass medial to the descending duodenum, and a gas-filled duodenum.
8. Describe the ultrasonic changes associated with pancreatitis.
Ultrasound changes include pancreatic swelling, increased echogenicity of the pancreas, and, less frequently, a mass effect in the area of the pancreas.
9. Are elevations in serum amylase and lipase activities definitive for the diagnosis of pancreatitis?
No. Neither enzyme is pancreas-specific; both are also produced by gastric and intestinal mucosal cells. Furthermore, because both enzymes are eliminated through the urine, a decrease in renal perfusion results in elevations of both enzymes. Finally, the administration of dexamethasone to dogs causes significant elevations in lipase without histologic evidence of pancreatitis.
10. Do normal lipase and amylase values eliminate the possibility of pancreatitis?
No. Many dogs and even more cats have confirmed pancreatitis with normal levels of both enzymes. Normal enzyme values in animals with pancreatitis may be due to impairment in pancreatic perfusion, depletion of stored enzymes, and / or disruption of the synthesis of new enzymes.
11. How is the diagnosis of pancreatitis confirmed?
Other than by histology, pancreatitis cannot be diagnosed on the basis of one test result. Common laboratory findings include leukocytosis, hyperglycemia, hypocalcemia, and elevations in amylase and lipase. Elevations in trypsin-like-immunoreactivity (TLI) correlate well with pancreatitis in both dogs and cats but also are affected by renal perfusion; furthermore, results generally take several days to return. Abdominal fluid analysis — in particular, lipase levels higher than serum lipase values — helps to make a case for pancreatitis. Ultrasound is useful for identifying an enlarged, inflamed pancreas. Diffuse or focal hypoechoic areas in the gland, along with compatible laboratory and physical findings, justify a high index of suspicion of pancreatitis.
12. How can the severity of acute pancreatitis be ascertained?
On admission it may not be easy to predict the severity or probable cause of acute pancreatitis. The clinician should be cognizant of concurrent laboratory abnormalities or clinical signs suggesting systemic complications. Examples include thrombocytopenia or clotting abnormalities, which may suggest disseminated intravascular coagulation (DIC); oliguria, which may indicate acute renal failure; hypotension and tachycardia, which may indicate systemic inflammatory response syndrome; and hypoglycemia, which may suggest sepsis.
13. What are the key components in treatment of pancreatitis?
The most important element of treatment is adequate fluid resuscitation. Decreased pancreatic perfusion due to hypovolemia, which may result from vomiting and third-space losses, may lead to progression of the disease if fluid therapy is inadequate. Recent studies suggest that colloid fluid resuscitation (plasma, hetastarch, and dextran 70) is an important component in the therapy of pancreatitis. In particular, fresh frozen plasma (10-20 ml / kg) is important in treatment of moderate-to-severe cases. Plasma as a colloid provides only small increases in oncotic properties but supplies clotting factors for management of disseminated intravascular coagulation and protease inhibitors that deactivate pancreatic enzymes in the systemic circulation. Prophylactic antibiotics, pain relief, antiemetics, and antacids are also important components of therapy. Studies in cats with experimentally induced acute hemorrhagic pancreatitis have shown that low-dose dopamine (5 mg / kg / min) reduces the severity of pancreatitis by reducing microvascular permeability. Dopamine as an adjunctive treatment awaits clinical evaluation.
14. How is fresh frozen plasma useful in the treatment of pancreatitis?
Studies in dogs suggest when alpha2-macroglobulin, one of the scavenger proteins for activated proteases in serum, is depleted, death rapidly ensues. Fresh frozen plasma (FFP) or fresh whole blood not only contains alpha2-macroglobulin but also albumin. Unfortunately, in a study of human pancreatitis patients, plasma failed to show any benefit. Incubating FFP with heparin may release antithrombin III and thus be useful in disseminated intravascular coagulation secondary to pancreatitis.
15. Is there evidence supporting the use of antibiotics or nonsteroidal antiinflammatory agents in pancreatitis?
No. Studies in humans have shown no benefit to antibiotics nor non-steroidal antiinflammatory agents. No data are available for the dog or cat.
16. What is the role of surgery in acute pancreatitis?
In most instances, pancreatitis is treated medically, and surgical intervention is not recommended. In patients that develop septic peritonitis or pancreatic abscess, however, surgery is the treatment of choice to remove necrotic tissue and to lavage the abdomen. Surgery also should be considered in patients who continue to deteriorate even with aggressive medical management.
17. What is done when the patient vomits every time food is offered?
Most patients with mild pancreatitis recover after avoidance of oral ingestion for 2 days, followed first by gradual introduction of water and then by small meals high in carbohydrates over the next few days. In patients that continue to vomit when offered food, one must first evaluate the case to ensure that no underlying disorder other than pancreatitis explains the persistent vomiting. In cases of smoldering pancreatitis, placement of a jejunostomy tube to provide nutrition with minimal stimulation of the pancreatitis should be strongly considered.
18. What are the long-term complications of pancreatitis?
Recurrent episodes of pancreatitis may result in progressive loss of pancreatic tissue and eventual development of diabetes mellitus and / or exocrine pancreatic insufficiency. Additional complications reported include acute fluid accumulation, infected necrosis, pancreatic pseudo-cyst formation, and pancreatic abscess.
19. Do corticosteroids cause severe pancreatitis?
Corticosteroids do not appear to cause pancreatitis, although they do increase serum lipase activity (but decrease serum amylase activity). Corticosteroid therapy is of no proven benefit in pancreatitis and may be harmful in severe pancreatitis.
20. Should food and water be withheld to allow the pancreas to rest and recover from the inflammatory episode?
Pancreatic rest has become the mainstay for treatment of acute pancreatitis, despite the absence of any clinical or experimental evidence to support this approach! Contrary to popular belief, pancreatic rest by avoiding pancreatic exocrine secretion has not made any impact on the clinical outcome of pancreatitis. Furthermore, no conclusive evidence to date indicates that medical treatment intended to decrease pancreatic exocrine secretion has any benefit, other than avoidance of pain, on the course of the disease. These observations are not surprising when one considers the fact that pancreatic exocrine secretion is severely impaired in an inflamed pancreas. If the pancreas is unable to respond to secretory stimuli, it makes perfect sense that therapeutic maneuvers to avoid pancreatic exocrine stimulation will have no bearing on the disease process.
21. Should total parenteral nutrition (TPN) be used in the treatment of pancreatitis?
In human patients, no difference in serum amylase activities between patients receiving total parenteral nutrition and controls is seen in the first 7 days after the diagnosis of acute pancreatitis. Although the total parenteral nutrition group achieved significantly greater nitrogen balance than controls, they also required significantly more days to first oral intake of clear liquids and full caloric intake. Most importantly, total parenteral nutrition patients experienced a significant prolongation of hospital stay (15 vs. 10 days in controls). No information is available in animals with pancreatitis.
22. Should total enteral nutrition (TEN) be used in the treatment of pancreatitis?
In human patients, total enteral nutrition moderates the acute-phase response and improves disease severity and clinical outcome despite unchanged pancreatic injury on computed tomography scan. Oxidant stress and systemic exposure to endotoxin also are reduced with total enteral nutrition. In humans, enteral feeding modulates the inflammatory and sepsis response in acute pancreatitis and is clinically beneficial. No information is available in animals with pancreatitis.