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Dr Manoj K Ghoda
Consultant Gastroenterologist
Clinical presentation
Abdominal pain:
It is the most prominent symptom, although not present in all
patients.
Pain is generally felt in the epigastrium, often with radiation to the
back.
Pain is boring, deep, and penetrating and may be associated with
nausea and vomiting. It may be relieved by sitting forward or
leaning forward, by assuming the knee-chest position on one side.
Pain may increase after a meal and is often nocturnal.
Initially pain may be episodic, often confused with an attack of
acute pancreatitis. With passage of time, pain may become more
continuous.
In some there may be more gradual onset of constant abdominal
pain, and
some may have no pain.
Weight loss:
Anorexia leading to weight loss and malnutrition.
May be seen during painful attacks, which prevent
adequate oral intake.
Weight loss may also occur owing to the
development of a concomitant disease such as
small bowel bacterial overgrowth or pancreatic or
extrapancreatic malignancy.
Steatorrhea:
Is a feature of far-advanced chronic pancreatitis.
Pancreatic lipase output decreases earlier and more substantially
compared to other pancreatic enzymes. As bicarbonate secretion
decreases in chronic pancreatitis and duodenal pH drops, lipase is
particularly inactivated.
It takes about 10-15 years before the exocrine deficiency becomes
manifest and it may be present in up to 80% of people after about 30
years of the disease.
These patients may present with diarrhea or weight loss but a large
number of watery stools is not a feature of chronic pancreatitis.
Stool may be bulky, foul-smelling with frank oil droplets
Fat-soluble vitamins deficiency may develop in patients with
pancreatic steatorrhea in a rare case.
Endocrine insufficiency:
Involves both insulin and glucagon with secondary diabetes.
Deficiency of both insulin and glucagon leads to a brittle
diabetes and insulin in these patients may lead to prolonged
and severe hypoglycemia.
Diabetes mellitus may become manifest within 10 years in
some patients but ultimately, 40-70% of patients will develop
diabetes after prolonged illness.
Diagnosis:
The diagnosis may be difficult in many cases
because lack of histological proof.
It has two aspects, one being the functional
aspect and the other being the structural aspect.
Both may be absent in early course of the
illness.
Evaluation of endocrine
functions:
Glucose tolerance test: This may show mild to
severe brittle diabetes
Structural diagnosis:
Plain X-ray abdomen:
May show diffuse pancreatic calcification.
It is more common in alcoholic, late-onset idiopathic,
hereditary, and tropical pancreatitis than in early-onset
idiopathic pancreatitis.
It may be absent in early phase of the disease. False
positives do occur.
USG:
USG findings indicative of chronic pancreatitis
include;
dilation of the pancreatic duct,
pancreatic ductal stones,
gland atrophy or enlargement, irregular gland
margins,
pseudocyst, and
changes in the parenchymal echo texture.
Sensitivity and specificity in the range of 5080%, with of 80- 90%.
CT:
More accurate than USG.
Changes are similar to USG findings.
MRI:
Comparable to CT, but with newer generation of
machine and faster protocols, congenital ductal
abnormalities could be picked up more
accurately
EUS:
EUS allows a highly detailed examination of the
pancreatic parenchyma and pancreatic duct.
Treatment:
Consists of the following,
Removing the underlying etiology.
Correcting the exocrine deficiency: This is
achieved by pancreatic supplements.
Medium chain triglycerides (MCT), which do not
require pancreatic lipase helps.
Correcting the endocrine deficiency: Oral
hypoglycemics and if required insulin for
diabetes.
Lastly.
Complications like pseudocyst or malignancy
are tackled appropriately.
ERCP may be useful in selected cases of
obstructive chronic pancreatitis, pancreatic
stricture and stones and certain congenital
abnormalities.
Surgery may be required in certain cases like
pseudocyst, difficult stones or extensive
calcification of pancreatic head, where a head
coring pancreatectomy may be required.