Chronic pancreatitisPresentation, investigations and medical

management

Dr Manoj K GhodaConsultant Gastroenterologist

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Gujarat Gastro Group

Clinical presentationAbdominal 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.

•The character, severity, and timing may change over a period.

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.

•Protein or carbohydrate digestion is not usually affected.

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.

Functional diagnosis (“Pancreatic function tests”):Evaluation of Exocrine function:

•Fecal fat estimation: A 72-hour measurement of fecal fat excretion is the gold standard but it is abnormal in advanced disease only. A 72-hour collection of stool while the patient is consuming a 100 g/day fat diet; should show fecal fat excretion to be less than 7 g of fat. Although, it must be said that, it has never become popular.

•The qualitative analysis of fecal fat can also be performed with a Sudan III stain of a random specimen of stool. More than six globules per high-power field is considered to be positive. It is positive only in patients with substantial steatorrhea.

•The pancreolauryl test measures the presence of pancreatic arylesterases within the gut lumen. It is accurate only in advanced chronic pancreatitis, with sensitivities of 80- 100%.

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 50-80%, 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.

Pancreatic enzyme replacement therapy (PERT) is indicated for patients who;

• loose weight,

•those with daily fecal fat excretion exceeding 7 to 15 grams while on a diet that contains 100 grams of fat per day, and

•those with clinically significant symptoms of steatorrhea.

The goals of pharmacotherapy are

• to improve the digestion and absorption of nutrients, •to reduce morbidity, and •to prevent complications

The Cystic Fibrosis Foundation provides guidance for weight-based enzyme dosing that recommends

• 1000 lipase units per kilogram per meal for children under 4 years of age and 500 units per kilogram per meal for those 4 years and older.

•Older patients may require lower doses of lipase units per kilogram per meal since they weigh more, but are likely to ingest less fat per kilogram.

•Half the standard dose is given with snacks, and the total daily dose should be based on approximately 3 meals and 2 to 3 snacks per day.5

•It is estimated that a dose of 50,000 IU of lipase per day will result in a 45% decrease in steatorrhea, while decreases of 60% to 70% are expected for patients taking 100,000 IU and 150,000 IU, respectively.

• “best way to take the enzymes is throughout the meal or at the beginning, during, and end of the meal so they mix as much as they can with the food and travel along the digestive system with the food.”

•Pain is controlled with appropriate analgesics.

•Simple analgesics are started first but morphine or its derivatives may also be required but there is a real danger of developing addiction.

•Celiac plexus block may help in selected patients.

•If there are stones or strictures, appropriate consultation may be obtained to see if, tackling these could offer any improvement in the pain.

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.

This lecture and many more interesting GI topics are available on our facebook account

Gujarat Gastro Group

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