Chronic Pancreatitis
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Introduction
Chronic pancreatitis is characterized by irreversible morphologic changes causing pain and/or loss of function
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Causes and Risk Factors
Alcohol accounts for 70-80% of chronic pancreatitis.
Idiopathic disease is responsible for about 20% of cases in the West, with other causes including cyctic fibrosis or other hereditary gene mutations, systemic lupus erythramtosis, autoimmune pancreatitis, trauma and metabolic disturbances such as hypercalcemia and hyperlipidemia. Cacific pancreatitis of the tropics is a major cause of disease worldwide.
Pathophysiology
Alcoholic pancreatitis is the result of abnormal secretion of acinar cells. Increased protein and calcium secretion, along with decreased bicarbonate secretion, leads to protein-calcium complexes which precipitate and obstruct ductules. Progressive blockage leads to l deterioration of pancreatic structures. Alcohol also appears to have direct cytotoxic effects, leading to bouts of acute inflammation and necrosis. The fibrosis that follows obstructs glands and ducts.
Signs and Symptoms
Some people with chronic pancreatitis are asymptomatic; others can have signficiant pain, while for others, manifestations of exocrine and endocrine insufficiency can preside.
- history
- physical exam
History
Pain
Ch: Knifelike, gripping
L: epigastric
O: initially after meals; may become continuous
R: to back
I: severe
D: initially may be episodic (20-30 minutes), but then can become constant
E: pancreatic insufficiency (diabetes, fat malabsorption)
P: worse with eating
P: fasting early
Diarrhea and weight loss can occur.
Physical Exam
People can look malnourished.
Investigations
- lab investigations
- diagnostic imaging
Lab Investigations
Pancreatic function tests can be used to provide a reasonable correlation with structural detioration. However, amylase and lipase may be normal even during well-established chronic pancreatitis, and as such can neither confirm nor exclude diagnosis.
The secretin stimulation test uses the fact that bicarbonate secretion is lowered in pancreatitis. IV secretin is given, and pancreatic juices are measured using an duodenal catheter. However, this is a labor-intensive and uncomfortable test and is not widely used.
Other less invasive and less accurate tests include 72 hour fecal fat to assay for steatorrhea, which is neither sensitive nor specific. Serum trypsinogen levels can also be used to measure exocrine insufficiency.
Diagnostic Imaging
MRI will show typical ductal changes, and CT can show calcifications. Use these to rule out pancreatic cancers.
Findings suggesting chronic pancreatitis include ductal abnormalities (dilation, stones), parenchymal abnormalities (calcification, atrophy, inhomogeneity), gland contour changes, and pseudocysts.
Plain films can be used to detect calcifications, alothough CT is more sensitive.
ERCP, MRCP, and endoscopic ultrasonography are the best modalities to evaluate structural problems.
Differential Diagnosis
Treatments
The main goal in caring for chronic pancreatitis is pain management, and is accomplished in a stepwise approach.
Alcohol cessation is the first order, followed by pancreatic enzyme supplementation to reduce pancreatic stimulus and then opiod analgesia.
Pancreatic enzyme preparations are also used to correct malabsorption and are used if people lose more than 10% of their body weight, excrete more than 15g/daily of fat in their stool, or develop dyspepsia.
Patients should eat 3 main meals daily along with three snacks. 25,000-50,000 IU of lipase should be taken simultaneously with the meal.
Acid-stable, encapsulated microspheres have greatly increased efficacy.
Medium-chain triglycerides, which do not need to be enzymatically digested, can also be taken to improve caloric intake. However, MCTs do not taste good and are unpopular.
Consequences and Course
Complications
Pancreatic insufficiency can occur, with fat malabsorption and ADEK problems, along with diabetes mellitus after 80-90% of the pancreas is damaged.
Pancreatic pseudocysts can develop, leading to fluid collection of pancreatic juices due to duct disruption. Fistulas, biliary obstruction, pancreatic cancer, small bowel bacterial overgrowth, and gastric varices following splenic vein thrombosis are also possible.
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Additional Resources
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