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CHRONIC PANCREATITIS,
ETIOLOGY & MANAGEMENT
Presentor: Dr Abinash Mishra
Chairperson : Prof & HOD Dr.Chitta Ranjan Panda Sir
Moderator: Dr Prasanta Kumar Parida sir
• Chronic Pancreatitis is a disease of the pancreas in which
recurrent inflammatory episodes result in replacement of the
pancreatic parenchyma by fibrous connective tissue.
• This fibrotic reorganisation of the pancreas leads to Pain,
Progressive Exocrine and Endocrine pancreatic insufficiency
PROGNOSIS OF ALCOHOLIC CP- 9,13,20
• The prognosis of Alcoholic Chronic Pancreatitis is relatively poor, and mortality is
generally greater than that seen in Chronic Pancreatitis of other etiologies.
• Diffuse Pancreatic Calcifications developed in 59% at a median of 8.7 years after
diagnosis .
• Exocrine Insufficiency developed in 48% of patients at a median of 13.1 years after
presentation .
• Endocrine Insufficiency developed in 38% after a median of 19.8 years after
presentation .
• Smoking is common in patients with alcohol-induced chronic pancreatitis, is
associated with an increased risk for pancreatic calcifications, Pancreatic Cancer &
Mortality in CP.
• Smoking & Alcohol cessation decreases the Progression of exocrine & Endocrine
Insufficiency.
Prospective study of alcohol drinking, smoking, and pancreatitis: the multiethnic cohort. Pancreas 2016,
Courses of early- and late-onset idiopathic and alcoholic chronic pancreatitis. Gastroenterology 1994
IDIOPATHIC CHRONIC PANCREATITIS-
IDIOPATHIC CP accounts upto 30% cases World wide , 60 % cases in India .
In India now a days Alcoholic & Tobacco Related CP increasing in prevalence.
Tropical Calcific Pacreatitis (FCPD) , Early Onset ICP , Late Onset ICP.
Early Onset ICP
Mean age at onset of around 20 years .
Pain found in almost 97 % patients.
The mean time to Calcification is 25 years, Exocrine Insufficiency 26 years, Endocrine
insufficiency 27.5 years.
Late Onset ICP
Median Age at Onset is 56 years.
Pain found in 54% pateints.
Mean time for Exocrine Insufficiency 16.9, Endocrine Insufficiency 11.9 years
Current Opinion Gastroenterology 2017;
Gastroenterology 1994
TROPICAL PANCREATITIS-
● Most commonly Found in South India
( few cases reported in Africa & Brazil)
● Disease of Youth .
● Mean Age is 24 years .
(>90% pateints present before 40 years )
● Prevalance in South India 1: 500 .
● It accounts 70 % of all cases of CP in South India .
● Recent studies Describes Alcohol & Smoking are gradually becoming the most common CP in India.
● Present as Abdominal pain, severe malnutrition, and exocrine or endocrine insufficiency.
● Large pancreatic calculi with marked dilation of the main pancreatic duct and gland atrophy develop in
more than 90% of patients.
● Pathogenesis : Unknown , Multifactorial (Cassava decreases RHODANESE, viral ,parasitic infections,
Deficiency of Micronutrients, Genetic Mutations)
The Indian Pancreatitis Study Group, Kerala State; 2006
Garg PK, Narayana D, Glob Health Epidemiol Genom 2016 OCT
RECURRENT ACUTE PANCREATITIS LEADING
TO CHRONIC PANCREATITIS-
● 10% OF AP , 36% OF RECURRENT AP cuases CP
● HYPERTRIGLYCERIDEMIA( triglyceride values greater than 1000 mg/dL
can produce acute pancreatitis & may be recurrent)
● DIABETES Mellitus , Hypercalcemia (rarely cause AP)
● Ischemia may result from vasculitis (e.g., SLE, polyarteritis nodosa),
atheromatous embolization of cholesterol plaques after transabdominal
aortography,Intraoperative hypotension, Hemorrhagic shock, ergotamine
overdose, and transcatheter arterial catheter embolization for hepatocellular
carcinoma.
● Necrotizing Biliary Pancreatitis has high Chance of Going to CP.
SAPE Model : Sentinel Acute Pancreatitis event-
ABDOMINAL PAIN IN CHRONIC PANCREATITIS-
● Abdominal pain is the Most Common clinical problem in patients with CP ( Almost Half
patients of CP needs Opoids for Pain Relief )
● Epigastric Pain, often with Radiation to the back.
● Pain is usually described as Boring, Deep, and Penetrating
● Associated with Nausea and Vomiting.
● Pain may be Relieved by sitting forward or leaning forward, by assuming the knee-chest
position on one side, or by squatting and clasping the knees to the chest.
● Pain Worsen after a meal and often is nocturnal.
● MECHANISM OF PAIN-
(1) increased pressure, ischemia, and inflammation in the pancreas,
(2) injury to and alterations in function of peripheral and central nociceptive nerves.
(3)Hyperstimulation of the pancreas via CCK has also been postulated as a potential cause
of pain.
case-control study from the North American Pancreatitis Study 2 cohort.
Pancreas 2013
PAIN MANAGEMENT IN CHRONIC PANCREATITIS
• Pain is the most common , most debilitating symptom & the one most often requiring
medical care.
• Most patients needs Medical management for Pain(Mostly Narcotics)(Few need
Acetaminophen or Aspirin)
• Addiction to Anagesics in CP patients is in 30% of the cases & May be higher.
• Single Physician ApproachStrategies to minimize the risk of overuse of narcotics and
addiction include having a single physician take responsibility for prescriptions, ongoing
counseling, monitoring of prescriptions, and regular clinic visits
• High dosages of Tramadol are equivalent to oral morphine in treating chronic pancreatitis,
with less Side Effects.
• Tramadol started with 50 mg BD may be increased to 100 mg TDS.
• Alcohol & Smoking Cessation has to be counseled in every Patients.
• Before Establishing as CP pain : Rule out Other causes of Abdominal Pain.
PANCREATIC ENZYMES IN PAIN MANAGEMENT-
• Use of Protease to reduce pain is via feed back inhibition by reducing pancreatic
secretion.
• Delivering Protease to Duodenum or Proximal Jejunum suppress CCK releasing Factors
which Inhibit CCK.
• Higher CCK stimulate the Pancreas to produce Pancreatic Secretion with Ductal
Obstruction leads to ductal pressure leading to enzymes into Duodenum.
• A Total dose of 150,000 units of Protease in 4 divided dose may be used.
• Best Response seen in Less Advanced Disease (without a Dilated Pancreatic Duct,
Calcifications, & Steatorrhea), Women, and Patients with Idiopathic Chronic Pancreatitis
.
• Less role in Advaced CP.
• Non Enteric coated Tablets are Preferred over Enteric coated Tablets because they are
released in Duodenum.
• Role of Protease in Pain Management is controversial.
ENDOSCOPIC THERAPY
FOR PAIN MANAGEMENT-
• The primary goal of Endoscopic therapy is to improve drainage of the Pancreatic Duct by relieving
ductal obstruction. Endoscopic therapy is limited to a subgroup of patients with amenable pancreatic
ductal anatomy. PD > 5 mm with Single or Dominant Stricture or Stone in Head.
• Pancreatic sphincterotomy, Stent placement, and Stone extraction ( or with Lithotripsy )
• Stricture or Calculi in Body & Tail are not amenable to ENDOSCOPY Therapy.
• PD stenting (successful placement of the stent) in close to 90% and pain improvement in about one
half to two thirds of patient .
• Complications seen in 20 % ( Stent Block , Migration, Perforation ) . Mortality seen in 0.6% .
• ESWL may be used in Patients where Endoscopy procedures are not Feasible.(Like Stone in body &
Tail of Pancreas)
Pancreas 2016
Digestive Endoscopy 2018
MANAGEMENT OF EXOCRINE & ENDOCRINE INSUFFICIENCY-
● Pancreatic Lipase secretion is reduced to less than 10% of the maximum output for PEI .
Steatorrhea is therefore a feature of far-advanced chronic pancreatitis, in which most of the
acinar cells have been Damaged. Fat Maldigestion occur 1st.
● Azotorrhea (protein maldigestion) also occurs when secretion of Proteases is less than 10%
of normal.
● With Advanced Disease Fat, Protein & Carbohydrate malabsorption occur.
● Even when there is significant loss of fat in stool, most patients pass only 3 or 4 stools daily
and some may pass only one.
● Deficiency of Fat Soluble Vitamins ,Water Soluble Vitamins & Micronutrients occur.
● Vit D deficiency leading to osteopenia in 40% of patients and osteoporosis in another 25%
of patients with CP and steatorrhea .
● Exocrine insufficiency in CP associated with increased Mortality.
Median time to development of Exocrine Insufficiency was
• 13.1 years in alcoholic chronic pancreatitis,
• 16.9 years in patients with late-onset ICP
• 26 years in patients with early-onset ICP
EXOCRINE INSUFFICIENCY
Journal of Clinical Gastroenterology 2018
Exocrine pancreatic insufficiency and malnutrition in CP . Pancreas 2018
MANAGEMENT OF EXOCRINE PANCREATIC
INSUFFICIENCY (EPI)-
• Up to 80% patients will develop PEI during their Life time.
• Diagnosis often made on History Fecal Elastase Test & 72 Hour Fecal Fat Analysis .
• Goal of Steatorrhea Management is ensuring atleast 90000 Units of Lipase with each
Meal.
• Once EPI diagnosed Starting Dose of 25000 to 50000 Lipase per Meal with Upward
Titration By Time.
• Most Patients of CP with EPI are under treated.( due to cost factor & number of pills
per day )
• Dose of Capsule needs to be increased by time.It can be increased to 90,000 per
Meal.
• If still Steatorrhea persists other Malabsorption syndromes needs to be ruled out Like
Celiac disease, or SIBO .
PANCREATIC ENDOCRINE INSUFFICIENCY
1. Islet cells appear to be relatively resistant to destruction in CP . So Mechanism is
complex.
2. Type 3c diabetes is characterized by low levels of insulin and low counter-
regulatory hormones (particularly glucagon and pancreatic polypeptide), rarely
ketosis, and frequent treatment induced hypoglycemia.
3. About 50% of Patients with Chronic Pancreatitis who develop diabetes will
require insulin.
Median times to development of Diabetes
Alcoholic CP 19.8,
Late-onset idiopathic CP 11.9
Early-onset idiopathic CP 27.5 years,
PANCREATIC ENDOCRINE INSUFFICIENCY
MANAGEMENT-
● FBS & PPBS measurement for Insulin Titration. HBA1C Monitoring every 3
months.
● Patients with Pancreatic Diabetes (Type 3c) has decreased Insulin & Glucagon due
to Pancreatic destruction leading to Risk of Hypoglycemia during Treatment.
● To know pancreatic Residual function of Beta Cell Fasting C Peptide needs to be
Measured.
● Diabetes mellitus is an independent predictor of mortality in patients with chronic
pancreatitis due to
● Progressive Microangiopathic complications or treatment-induced hypoglycemia.
● Appropriate monitoring for Nephropathy (urine ACR) , Retinopathy(Fundoscopy),
and neuropathy(NCS) is indicated.
COMPLICATIONS IN CHRONIC PANCREATITIS-
1)Pseudocyst occur in about 25% of patients with chronic pancreatitis, and are most
commonly seen in Alcoholic CP.Management is via conservative, surgical,
percutaneous, or endoscopic Therapy.
2)GI BLEEDING Pancreatic causes (Pseudocyst, Pseudoaneurysm, and Portal or
Splenic Vein Thrombosis)
3)Psuedo Anuerysm ( seen in upto 21% patients)
4)Variceal Bleed due to Splenic Vein Thrombosis.
5)Bile duct obstruction & Duodenal Obstruction ( Due to Fibrosis in Head )
6)Fistulas (External & Internal)
7)Pancreatic Malignancies
8)Dysmotility.
TAKE HOME MESSAGES
1) Finding the etiology & Its management is very Important in Preventing progression
of Disease.
2) Tests for Diagnosis of CP & It's Severity.
3) Managing Pain in CP with Opoids ( Tramadol ) & Adding Antidepressants Early to
Decrease Pain Threshold .
4) Uncoated Protease 1,50,000 needed For Pain Management & Still Controversial .
5) Antioxidants needs to be added in Pain Management & Further Progression of
Disease.
6) ERCP, ESWL,Surgical Therapy whenever Indicated .
7) Tests for Exocrine Insufficiency like History, Fecal Elastase,72 hour fecal Fat & Its
management.
8) Tests for Endocrine Insufficiency via HbA1C , C Peptide & Its management via
Insulin & awareness about Hypoglycemia.
9) Giving Importance to Diet .(Medium Chain Triglyceride Diet & Mediterranean Diet)
10) Early diagnosis & Managing the Complications of CP .
chronic pancreatitis .pptx

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chronic pancreatitis .pptx

  • 1. CHRONIC PANCREATITIS, ETIOLOGY & MANAGEMENT Presentor: Dr Abinash Mishra Chairperson : Prof & HOD Dr.Chitta Ranjan Panda Sir Moderator: Dr Prasanta Kumar Parida sir
  • 2. • Chronic Pancreatitis is a disease of the pancreas in which recurrent inflammatory episodes result in replacement of the pancreatic parenchyma by fibrous connective tissue. • This fibrotic reorganisation of the pancreas leads to Pain, Progressive Exocrine and Endocrine pancreatic insufficiency
  • 3.
  • 4.
  • 5.
  • 6.
  • 7.
  • 8. PROGNOSIS OF ALCOHOLIC CP- 9,13,20 • The prognosis of Alcoholic Chronic Pancreatitis is relatively poor, and mortality is generally greater than that seen in Chronic Pancreatitis of other etiologies. • Diffuse Pancreatic Calcifications developed in 59% at a median of 8.7 years after diagnosis . • Exocrine Insufficiency developed in 48% of patients at a median of 13.1 years after presentation . • Endocrine Insufficiency developed in 38% after a median of 19.8 years after presentation . • Smoking is common in patients with alcohol-induced chronic pancreatitis, is associated with an increased risk for pancreatic calcifications, Pancreatic Cancer & Mortality in CP. • Smoking & Alcohol cessation decreases the Progression of exocrine & Endocrine Insufficiency. Prospective study of alcohol drinking, smoking, and pancreatitis: the multiethnic cohort. Pancreas 2016, Courses of early- and late-onset idiopathic and alcoholic chronic pancreatitis. Gastroenterology 1994
  • 9. IDIOPATHIC CHRONIC PANCREATITIS- IDIOPATHIC CP accounts upto 30% cases World wide , 60 % cases in India . In India now a days Alcoholic & Tobacco Related CP increasing in prevalence. Tropical Calcific Pacreatitis (FCPD) , Early Onset ICP , Late Onset ICP. Early Onset ICP Mean age at onset of around 20 years . Pain found in almost 97 % patients. The mean time to Calcification is 25 years, Exocrine Insufficiency 26 years, Endocrine insufficiency 27.5 years. Late Onset ICP Median Age at Onset is 56 years. Pain found in 54% pateints. Mean time for Exocrine Insufficiency 16.9, Endocrine Insufficiency 11.9 years Current Opinion Gastroenterology 2017; Gastroenterology 1994
  • 10. TROPICAL PANCREATITIS- ● Most commonly Found in South India ( few cases reported in Africa & Brazil) ● Disease of Youth . ● Mean Age is 24 years . (>90% pateints present before 40 years ) ● Prevalance in South India 1: 500 . ● It accounts 70 % of all cases of CP in South India . ● Recent studies Describes Alcohol & Smoking are gradually becoming the most common CP in India. ● Present as Abdominal pain, severe malnutrition, and exocrine or endocrine insufficiency. ● Large pancreatic calculi with marked dilation of the main pancreatic duct and gland atrophy develop in more than 90% of patients. ● Pathogenesis : Unknown , Multifactorial (Cassava decreases RHODANESE, viral ,parasitic infections, Deficiency of Micronutrients, Genetic Mutations) The Indian Pancreatitis Study Group, Kerala State; 2006 Garg PK, Narayana D, Glob Health Epidemiol Genom 2016 OCT
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  • 12. RECURRENT ACUTE PANCREATITIS LEADING TO CHRONIC PANCREATITIS- ● 10% OF AP , 36% OF RECURRENT AP cuases CP ● HYPERTRIGLYCERIDEMIA( triglyceride values greater than 1000 mg/dL can produce acute pancreatitis & may be recurrent) ● DIABETES Mellitus , Hypercalcemia (rarely cause AP) ● Ischemia may result from vasculitis (e.g., SLE, polyarteritis nodosa), atheromatous embolization of cholesterol plaques after transabdominal aortography,Intraoperative hypotension, Hemorrhagic shock, ergotamine overdose, and transcatheter arterial catheter embolization for hepatocellular carcinoma. ● Necrotizing Biliary Pancreatitis has high Chance of Going to CP.
  • 13. SAPE Model : Sentinel Acute Pancreatitis event-
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  • 19. ABDOMINAL PAIN IN CHRONIC PANCREATITIS- ● Abdominal pain is the Most Common clinical problem in patients with CP ( Almost Half patients of CP needs Opoids for Pain Relief ) ● Epigastric Pain, often with Radiation to the back. ● Pain is usually described as Boring, Deep, and Penetrating ● Associated with Nausea and Vomiting. ● Pain may be Relieved by sitting forward or leaning forward, by assuming the knee-chest position on one side, or by squatting and clasping the knees to the chest. ● Pain Worsen after a meal and often is nocturnal. ● MECHANISM OF PAIN- (1) increased pressure, ischemia, and inflammation in the pancreas, (2) injury to and alterations in function of peripheral and central nociceptive nerves. (3)Hyperstimulation of the pancreas via CCK has also been postulated as a potential cause of pain. case-control study from the North American Pancreatitis Study 2 cohort. Pancreas 2013
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  • 21. PAIN MANAGEMENT IN CHRONIC PANCREATITIS • Pain is the most common , most debilitating symptom & the one most often requiring medical care. • Most patients needs Medical management for Pain(Mostly Narcotics)(Few need Acetaminophen or Aspirin) • Addiction to Anagesics in CP patients is in 30% of the cases & May be higher. • Single Physician ApproachStrategies to minimize the risk of overuse of narcotics and addiction include having a single physician take responsibility for prescriptions, ongoing counseling, monitoring of prescriptions, and regular clinic visits • High dosages of Tramadol are equivalent to oral morphine in treating chronic pancreatitis, with less Side Effects. • Tramadol started with 50 mg BD may be increased to 100 mg TDS. • Alcohol & Smoking Cessation has to be counseled in every Patients. • Before Establishing as CP pain : Rule out Other causes of Abdominal Pain.
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  • 24. PANCREATIC ENZYMES IN PAIN MANAGEMENT- • Use of Protease to reduce pain is via feed back inhibition by reducing pancreatic secretion. • Delivering Protease to Duodenum or Proximal Jejunum suppress CCK releasing Factors which Inhibit CCK. • Higher CCK stimulate the Pancreas to produce Pancreatic Secretion with Ductal Obstruction leads to ductal pressure leading to enzymes into Duodenum. • A Total dose of 150,000 units of Protease in 4 divided dose may be used. • Best Response seen in Less Advanced Disease (without a Dilated Pancreatic Duct, Calcifications, & Steatorrhea), Women, and Patients with Idiopathic Chronic Pancreatitis . • Less role in Advaced CP. • Non Enteric coated Tablets are Preferred over Enteric coated Tablets because they are released in Duodenum. • Role of Protease in Pain Management is controversial.
  • 25. ENDOSCOPIC THERAPY FOR PAIN MANAGEMENT- • The primary goal of Endoscopic therapy is to improve drainage of the Pancreatic Duct by relieving ductal obstruction. Endoscopic therapy is limited to a subgroup of patients with amenable pancreatic ductal anatomy. PD > 5 mm with Single or Dominant Stricture or Stone in Head. • Pancreatic sphincterotomy, Stent placement, and Stone extraction ( or with Lithotripsy ) • Stricture or Calculi in Body & Tail are not amenable to ENDOSCOPY Therapy. • PD stenting (successful placement of the stent) in close to 90% and pain improvement in about one half to two thirds of patient . • Complications seen in 20 % ( Stent Block , Migration, Perforation ) . Mortality seen in 0.6% . • ESWL may be used in Patients where Endoscopy procedures are not Feasible.(Like Stone in body & Tail of Pancreas) Pancreas 2016 Digestive Endoscopy 2018
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  • 27. MANAGEMENT OF EXOCRINE & ENDOCRINE INSUFFICIENCY-
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  • 29. ● Pancreatic Lipase secretion is reduced to less than 10% of the maximum output for PEI . Steatorrhea is therefore a feature of far-advanced chronic pancreatitis, in which most of the acinar cells have been Damaged. Fat Maldigestion occur 1st. ● Azotorrhea (protein maldigestion) also occurs when secretion of Proteases is less than 10% of normal. ● With Advanced Disease Fat, Protein & Carbohydrate malabsorption occur. ● Even when there is significant loss of fat in stool, most patients pass only 3 or 4 stools daily and some may pass only one. ● Deficiency of Fat Soluble Vitamins ,Water Soluble Vitamins & Micronutrients occur. ● Vit D deficiency leading to osteopenia in 40% of patients and osteoporosis in another 25% of patients with CP and steatorrhea . ● Exocrine insufficiency in CP associated with increased Mortality. Median time to development of Exocrine Insufficiency was • 13.1 years in alcoholic chronic pancreatitis, • 16.9 years in patients with late-onset ICP • 26 years in patients with early-onset ICP EXOCRINE INSUFFICIENCY Journal of Clinical Gastroenterology 2018 Exocrine pancreatic insufficiency and malnutrition in CP . Pancreas 2018
  • 30. MANAGEMENT OF EXOCRINE PANCREATIC INSUFFICIENCY (EPI)- • Up to 80% patients will develop PEI during their Life time. • Diagnosis often made on History Fecal Elastase Test & 72 Hour Fecal Fat Analysis . • Goal of Steatorrhea Management is ensuring atleast 90000 Units of Lipase with each Meal. • Once EPI diagnosed Starting Dose of 25000 to 50000 Lipase per Meal with Upward Titration By Time. • Most Patients of CP with EPI are under treated.( due to cost factor & number of pills per day ) • Dose of Capsule needs to be increased by time.It can be increased to 90,000 per Meal. • If still Steatorrhea persists other Malabsorption syndromes needs to be ruled out Like Celiac disease, or SIBO .
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  • 32. PANCREATIC ENDOCRINE INSUFFICIENCY 1. Islet cells appear to be relatively resistant to destruction in CP . So Mechanism is complex. 2. Type 3c diabetes is characterized by low levels of insulin and low counter- regulatory hormones (particularly glucagon and pancreatic polypeptide), rarely ketosis, and frequent treatment induced hypoglycemia. 3. About 50% of Patients with Chronic Pancreatitis who develop diabetes will require insulin. Median times to development of Diabetes Alcoholic CP 19.8, Late-onset idiopathic CP 11.9 Early-onset idiopathic CP 27.5 years,
  • 33. PANCREATIC ENDOCRINE INSUFFICIENCY MANAGEMENT- ● FBS & PPBS measurement for Insulin Titration. HBA1C Monitoring every 3 months. ● Patients with Pancreatic Diabetes (Type 3c) has decreased Insulin & Glucagon due to Pancreatic destruction leading to Risk of Hypoglycemia during Treatment. ● To know pancreatic Residual function of Beta Cell Fasting C Peptide needs to be Measured. ● Diabetes mellitus is an independent predictor of mortality in patients with chronic pancreatitis due to ● Progressive Microangiopathic complications or treatment-induced hypoglycemia. ● Appropriate monitoring for Nephropathy (urine ACR) , Retinopathy(Fundoscopy), and neuropathy(NCS) is indicated.
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  • 36. COMPLICATIONS IN CHRONIC PANCREATITIS- 1)Pseudocyst occur in about 25% of patients with chronic pancreatitis, and are most commonly seen in Alcoholic CP.Management is via conservative, surgical, percutaneous, or endoscopic Therapy. 2)GI BLEEDING Pancreatic causes (Pseudocyst, Pseudoaneurysm, and Portal or Splenic Vein Thrombosis) 3)Psuedo Anuerysm ( seen in upto 21% patients) 4)Variceal Bleed due to Splenic Vein Thrombosis. 5)Bile duct obstruction & Duodenal Obstruction ( Due to Fibrosis in Head ) 6)Fistulas (External & Internal) 7)Pancreatic Malignancies 8)Dysmotility.
  • 37. TAKE HOME MESSAGES 1) Finding the etiology & Its management is very Important in Preventing progression of Disease. 2) Tests for Diagnosis of CP & It's Severity. 3) Managing Pain in CP with Opoids ( Tramadol ) & Adding Antidepressants Early to Decrease Pain Threshold . 4) Uncoated Protease 1,50,000 needed For Pain Management & Still Controversial . 5) Antioxidants needs to be added in Pain Management & Further Progression of Disease. 6) ERCP, ESWL,Surgical Therapy whenever Indicated . 7) Tests for Exocrine Insufficiency like History, Fecal Elastase,72 hour fecal Fat & Its management. 8) Tests for Endocrine Insufficiency via HbA1C , C Peptide & Its management via Insulin & awareness about Hypoglycemia. 9) Giving Importance to Diet .(Medium Chain Triglyceride Diet & Mediterranean Diet) 10) Early diagnosis & Managing the Complications of CP .