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- 1. CHRONIC PANCREATITIS Presentation By: Dr. Sarthak Kansal Guides: Dr. Sharath Chandra BJ
- 2. INTRODUCTION: • Chronic pancreatitis (CP) is a serious disorder which can have a severe impact on quality of lifein addition to life-threatening long-term sequelae • Incidence • Western population ranges from 8 to10 cases per year per 100,000 population, • Overall prevalence is 27.4 cases per 100,000 population. • Prevalence of chronic pancreatitis in Southern India is 114-200 cases per 100,000 population • Prognosis : Overall, 10-year survival is about 70%, and 20-year survival is about 45%.
- 3. Historical aspect: • Portal was the first to describe the clinical signs of chronic pancreatitis in 1803. • In 1815, Fleischman speculated about the potential role of excessive alcohol consumption. • Comfort coined the term “chronic relapsing pancreatitis” in 1946
- 4. DEFINITION: • Chronic pancreatitis refers to an ongoing inflammatory and fibrosing disorder characterised by irreversible morphologic changes, progressive and permanent loss of exocrine and endocrine function, and a clinical pattern of recurrent acute exacerbation or persistent pain. • a spectrum of inflammatory and fibrosing conditions • Recurrent episodes (or even a single episode) of acute pancreatitis may lead to chronic changes
- 5. Marseilles-Rome classification • Chronic obstructive pancreatitis is characterized by exocrine atrophy and is associated with duct stenosis caused by tumors, pseudocyst, or scarring from prior acute pancreatitis. • Chronic calcifying pancreatitis is characterized by intraductal calcifications and protein plugs, and is often associated with atrophy, stenotic ducts, and areas of acute inflammation or pseudocyst. • Chronic inflammatory pancreatitis consists of dense infiltration of mononuclear inflammatory cells.
- 6. •Chronic pancreatitis lacks a simple unifying theory of disease pathogenesis. •The precise mechanism by which any specific agent or circumstance induces pancreatitis remains obscure. •Chronic pancreatitis may present without prior acute attacks.
- 7. Risk Factor/Etiology • Given the lack of an identified, uniform pathogenic trigger, the concept of risk modifiers rather than etiologies or causes of chronic pancreatitis may be more appropriate in classifying the disease, particularly when making decisions regarding patient management. • Whitcomb has proposed the TIGAR-O system as a potential framework that allows various risk factors associated with the disease to be logically organized into categories.
- 8. TIGAR-O CLASSIFICATION OF CHRONIC PANCREATITIS Modified from Etemad B, Whitcomb DC. Chronic pancreatitis: diagnosis, classification, and new genetic developments. Gastroenterology. 2001;120:682
- 9. ALCOHOL AND PANCREATITIS • Excessive alcohol ingestion has been associated with chronic pancreatitis since the term was introduced by Comfort in 1946. • Alcohol use continues to be the most commonly identified environmental risk factor clinically. • Chronic pancreatitis in humans occurs in the absence of significant alcohol usage, and fewer than 5% of alcoholics actually develop pancreatic disease. • Chronic pancreatitis is not simply a “drunkard’s disease,” but rather is more appropriately attributed to a variety of genetic, environmental, anatomic, immunologic, and other poorly understood susceptibility factors that interact to initiate and perpetuate the pathology.
- 10. PATHOPHYSIOLOGY • Traditional theories of the pathogenesis of acute pancreatitis include the toxic-metabolic or oxidative stress hypothesis, in which normal acinar cell processing and release of zymogens are disrupted by a toxic or oxidative stressor. • The ductal obstruction hypothesis that proposes a mechanical role for ductal plugs and stones causing disruption of the integrity of the acinar cell (common in alcoholic and tropical disease).
- 11. In Mechanism of pancreatic fibrosis, the central histological feature that characterizes the evolution from acute disease to chronic pancreatitis. One attractive hypothesis is that a sentinel acute pancreatitis event (SAPE) primes the pancreas for fibrogenesis. Acute pancreatitis Local inflammatory cytokines Are released by macrophages Cytokines infiltrate the gland as well as resident pancreatic stellate cells, Myofibroblasts- anti-inflammatory mediators drive tissue cells and macrophages to synthesize and deposit fibrogenic matrix proteins.
- 12. CLINICAL PRESENTATION: Endocrine: • Pancreatic Diabetes- Type 3 c Diabetes • Global loss of insulin, glucagon and pancreatic polypeptide • Paradoxical combination of enhanced peripheral sensitivity to insulin and decrease hepatic sensitivity – Brittle Diabetes • Pain • Weight loss and malnutrition Exocrine: • Diarrhoea • Steatorrhea • Weight loss • Malnutrition Pancreatic Insufficiency
- 13. MANIFESTATION RELATED TO EXTRAPANCREATIC COMPLICATIONS: Intestinal or biliary obstruction due to compression by a pseudocyst progressive peripancreatic fibrosis and gastrointestinal hemorrhage due to blood lost into the pancreatic duct (hemosuccus pancreaticus) or due to rupture of pseudoaneurysm into a pseudocyst or, splenomesenteric vein thrombosis.
- 14. MECHANISM OF PAIN: • Pain results from capsular stretch associated with ductal or organ hypertension. • Pain represents a neuropathy caused by repeated inflammatory insults and damage to retroperitoneal sensory nerves. • Altered nociception of pain Recent evidence demonstrating neuroplasticity in nociceptive dorsal root ganglia in chronic inflammatory states, with evidence of upregulation of nociceptors such as TRPV1 by proteolytic enzymes such as trypsin, supports this theory
- 16. DIAGNOSIS: • Diagnosis is usually suspected based on an appropriate clinical history and is confirmed by imaging studies. • Laboratory investigation -serum amylase or lipase, • Elevation of liver function tests, particularly serum bilirubin and alkaline phosphatase, may indicate the presence of bile duct obstruction.
- 17. • For Steatorrhea- • Fecal-elastase-I value (<100microgram/g of stool) • 72 hour quantitative fecal fat is gold standard (>7gm/day is confirmatory) • Genetic Testing for CFTR and PRSS1 • Autoimmune pancreatitis- Inflammatory markers- ESR, CRP, ANA, RF, antibodies and immunoglobulins particularly IgG4
- 18. Transabdominal Ultrasonography Diagnostic criteria for CP by transabdominal US are • irregular contour (lobulation) • pancreatic duct dilation and irregularity of the main pancreatic duct, • loss or reduction of pancreatic parenchyma echogenicity (echo-poor or echo-rich areas) • cysts or cavities, • pancreatic calcifications
- 19. The most common CT findings • Dilated pancreatic duct (68%) • Parenchymal atrophy (54%) • Pancreatic calcifications (50%) Other Findings • Peripancreatic fluid collection • Focal Pancreatic enlargement • Biliary duct Dilation • Irregular pancreatic parenchyma contour CT:
- 20. CT is useful is assessing following Complications : • Pancreatic duct disruption • Pseudocysts • Portal and Splenic Vein thrombosis • Splenic and Pancreaticoduodenal artery pseudoaneurysms
- 21. MRI • Reliable alternative • Useful to Detects changes in the pancreatic parenchyma s/o chronic inflammation such as change in intensity, pancreatic atrophy and irregularities in the contour • MRCP with secretin injection is particularly useful to evaluate duct pathologies- intraductal strictures and pancreatic disruption
- 22. ERCP • “Gold standard” • Indications: for patients whom other diagnostic tests, including CT and MRCP are C/I or failed to corroborate the diagnosis • Therapeutic modality in pancreatic duct complications amendable to endoscopic therapy- stricture, stone, pseudocysts and biliary stenosis
- 23. EUS • Most accurate- in patients with (minimal change disease) MCD or in the early stages • Histological evidence of inflammation, atrophy, and fibrosis is the gold standard for the diagnosis of chronic pancreatitis
- 25. MANAGEMENT OF CHRONIC PANCREATITIS
- 26. Endocrine and Exocrine replacement therapy The main goal of the treatment of pancreatic exocrine dysfunction is to ensure that optimal amounts of lipase reach the duodenum with the delivered food. Uncoated preparation, enteric-coated tablets, enteric-coated microsphere preparations Enzyme preparations should contain sufficient lipase units, with 20,000 to 40,000 units as a starting dose for a meal and 10,000 to 20,000 lipase units for a snack
- 28. MEDICAL MANAGEMENT FOR PAIN NSAIDS OPOIDS LONG ANCTING NARCOTICS+/- SHORT ACTING NARCOTICS
- 29. CELIAC PLEXUS NEUROLYSIS AND BLOCK • AIM: either selectively destroying the celiac plexus or temporarily blocking visceral afferent nociceptors. • AGENTS USED: • alcohol or phenol for Neurolysis • bupivacaine and triamcinolone for a Temporary block. • METHOD: 20 ml of 50% ethanol is injected along each side of the aorta using 21-gauge spinal needle • Under computed tomography imaging, percutaneous ultrasound, fluoroscopy, or endoscopic ultrasound.
- 31. • Pancreatic ductal obstruction by fibrotic stenoses and/or calculi are the most frequent indications for endoscopic therapy. • aim to decompress and drain the pancreatic ductal system. INTERVENTIONAL AND ENDOSCOPIC THERAPY INDICATIONS:
- 34. SURGICAL TREATMENT • Indications for Surgery 1. Persisting pain intractable to pharmacotherapy is the main indication 2. severe malabsorption 3. suspicion of malignant transformation 4. multiple relapses 5. complications like pseudocyst, segmental portal hypertension; biliary obstruction (Wadsworth syndrome) 6. Pseudocyst 7. pancreatic ductal dilatation > 7 mm 8. pancreatic ascites/fistula 9. pancreatic ductal stenosis.
- 38. DRAINAGE PROCEDURES • Pancreatic duct sphincterotomy was one of the first surgical procedures proposed for patients with CP and stenosis at the papilla of Vater • The original Puestow procedure and its modification by Partington and Rochelle (1960) proved more successful in patients with CP and a dilated pancreatic duct. • Pancreatic malignancy and chronic pancreatitis are difficult to differentiate grossly and on table biopsy is a must.
- 42. Pure Drainage Operations: Laterolateral pancreaticojejunostomy: Partington-Rochelle procedure Ductal dilation > 7 mm, without inflammatory mass Caudal drainage: Puestow- procedure Rare indications, replaced by other procedures Cystojejunostomy Surgical procedure of choice for isolated pseudocysts Caution: Intraoperative frozen section to exclude a cystic neoplasm
- 45. Pylorus Preservation Partial Pancreaticoduodenectomy (Traverso Longmire)
- 48. Resection Procedures: Pancreatic Head Resections •Always include a ductal drainage •Procedures of choice if inflammatory mass in the head of the pancreas All techniques have comparable results Pancreatico- duodenectomy Pylorus preserving pancreaticodupdenectomy Procedure of choice in suspected malignancy and in irreversible duodenal stenosis
- 49. Duodenum-Preserving Pancreatic Head Resection: Beger Procedure-patients with CP and an inflammatory mass in the head of the pancreas
- 50. Duodenum-Preserving Pancreatic Head Resection: Frey Procedure-less severe inflammation in the head of the pancreas that is combined with an obstruction in the left-sided pancreatic duct.
- 51. Duodenum-Preserving Pancreatic Head Resection: Bern Modification -ideal for patients with an inflammatory mass and no stenosis in the left-sided duct
- 56. Islet Cell Auto-transplantation-The Mirkowitch technique • Total pancreatectomy and islet autotransplantation are done for chronic pancreatitis with intractable pain when other treatment measures have failed, allowing insulin secretory capacity to be preserved, minimising or preventing diabetes, while at the same time removing the root cause of the pain. • Pain relief is obtained in most patients, and insulin independence preserved long-term in about a third, with another third having sufficient beta-cell function so that the surgical diabetes is mild. • Islet autotransplantation should be used more widely to preserve beta-cell mass in major pancreatic resections .
- 58. REFERENCES • Shackelford’s Surgery of the Alimentary Tract- 8th edition • Sabiston Textbook of Surgery- 20th edition • Bailey and Love’s Short Practice of Surgery- 27th edition • Maingot’s Abdominal Operations -13th edition • Blumgart's Surgery of the Liver, Biliary Tract and Pancreas, 6th Edition
- 59. STATISTICS 0 50 100 150 200 250 300 2019 2020 2021 2022 CHRONIC PANCREATITIS STATISTICS FROM YEAR 2019 JSSH, MYSURU MALE FEMALE TOTAL
- 60. PANCREATIC SURGERY STATISTICS FROM YEAR 2019 JSSH, MYSURU YEAR Partial Pancreatectomy Whipple’s Procedure 2019 5 3 2020 4 6 2021 5 4 2022 NIL 4
- 61. THANK YOU
- 64. A pancreatic pseudocyst is defined as a fluid collection within or adjacent to the pancreas that becomes completely encapsulated with a mature, nonepithelialized, fibrous, inflammatory wall. PANCREATIC PSEUDOCYST
Editor's Notes
- However, in reality, acute and chronic pancreatitis represent more of a spectrum of inflammatory and fibrosing conditions of the pancreas than the two dichotomous terms would otherwise imply Recurrent episodes (or even a single episode) of acute pancreatitis may lead to chronic changes within the pancreas., although the timing and extent to which such changes merit a change in nomenclature to chronic pancreatitis is somewhat arbitrary.
- The marseilles rome classification further divides chronic pancreatitis into several morphological subtypes that may coexist in the same patient
- David c whitcomb
- TIGAR-O system reflects the fact that in chronic pancreatitis there is a diversity of etiologic risk factors that contributes to a spectrum of pathological and functional derangements, clinical features, and natural history. Toxic metabolic includes 55-80% of patients 20% of patients with chronic pancreatitis have no clinically obvious risk factors Genetic- ½ of hereditary pancreatitis patients are found to have mutations in cationic trypsinogen (PRSS1) gene- has a Autosomal dominant pattern of inheritance with a high degree of penetrance 90% of Cystic Fibrosis patients are pancreatic insufficient, linked to the mutation in the CF transmembrane conductance regulator (CFTR) gene, which shows autosomal recessive inheritance with incomplete penetrance Auto-immune pancreatitis AKA lymphoplasmocytic sclerosing pancreatitis is characterized by diffuse glandular enlargement and infiltration of CD4-CD8 positive lymphocytes and IgG4 positive plasma cells 20% autoimmune conditions are associated with CP like UC/CD, PBC, PSC An additional classification system uses the M-ANNHEIM paradigm: Multiple risk factors of Alcohol consumption (excessive >80 g/day, increased 20 to 80 g/ day, moderate <20 g/day), Nicotine consumption, Nutritional factors (high calorie proportion of fat and protein, hyperlipidemia), Hereditary factors, Efferent duct factors (pancreas divisum, annular pancreas, tumors, posttraumatic, sphincter of Oddi dysfunction), Immunologic factors and Miscellaneous and rare metabolic disorders (hypercalcemia, hyperparathyroidism, chronic renal failure, drugs, toxins)
- Chronic pancreatitis in humans occurs in the absence of significant alcohol usage, and fewer than 5% of alcoholics actually develop pancreatic disease
- Thus, following the SAPE, the local pancreatic environment may be permanently altered by the persistent presence of anti-inflammatory and profibrogenic cell populations that are perpetually activated by ongoing toxic-metabolic, oxidative, or mechanical stress. The pancreas then becomes subject to repeated cycles of inflammation and progressive fibrosis. Local inflammatory cytokines released during acute pancreatitis activate circulating macrophages that infiltrate the gland as well as resident pancreatic stellate cells, myofibroblast-like cells that are normally quiescent, myofibroblast-like cells during the subsequent healing phase
- 1. typically localizes to the left upper quadrant or epigastric region, often radiating around or into the back. The pattern of pain is variable. Some may experience recurrent attacks of moderate to severe pain interspersed with periods of relative or complete quiescence. In others, the pain may be persistent and lead to significant incapacitation and chronic disability. During acute exacerbations, the pain may be increased by food intake and is frequently associated with nausea and vomiting 2. due to both decreased intake as well as exocrine insufficiency
- On occasion, the initial manifestation of chronic pancreatitis will be related to extrapancreatic complications such as
- It is also acknowledged that certain forms of chronic pancreatitis can occur in the absence of pain
- The disease course can be classified in three distinct stages : Stage A is the early stage, characterized by recurrent acute attacks, with no or only mild impairment of pancreatic function. Stage B (moderate) comes later in the disease course, when complications are seen— pseudocysts, cholestasis, and segmental portal hypertension— along with increasing intensity of pain, more frequent acute painful attacks, and significantly impaired pancreatic function. Stage C (advanced) represents end-stage disease, characterized by less frequent episodes and less intense pain but with marked impairment of endocrine and exocrine pancreatic function (“burnout”)
- Laboratory investigation is of limited value. Acute exacerbation of abdominal pain may be paralleled by a transient increase in serum amylase or lipase, but these may be normal with progressive destruction of acinar cell mass.
- <100 severe exocrine pancreatic insufficiency 100-200 mild to moderate >200mcg is normal
- The major disadvantage of US is the occasional difficult examination based on poor visualization of the pancreas, mainly because of overlying gas-filled bowel loops, obesity, and technical and operator-dependent factors
- The diagnosis is confirmed by imaging studies, most commonly computed tomography (CT). THE CT FINDINGS DEPEND ON….. In the early phases of chronic pancreatitis, ductal or parenchymal changes may be rather subtle, but as the disease advances, progressive and irreversible changes in organ architecture are readily apparent.
- CT is useful to assess complications such as
- Gabapentin, SSRI,TCA, can also be tried
- Celiac plexus neurolysis and celiac block involve injecting an agent at the celiac axis with the aim of either selectively destroying the celiac plexus or temporarily blocking visceral afferent nociceptors. Agents most commonly used for this purpose include alcohol or phenol for neurolysis and bupivacaine and triamcinolone for a temporary block.
- 20 ml of 50% ethanol is injected along each side of the aorta using 21-gauge spinal needle. Methods to administer such agents to the celiac ganglion include computed tomography imaging, percutaneous ultrasound, fluoroscopy, or endoscopic ultrasound Splanchinectomy usually performed by a thoracoscopic approach has also been used but similar to other forms of neurolysis, permanent resolution of pain is unusual
- Patients with proximal stenosis and no calcifications or inflammatory mass may be treated endoscopically. If two to three repetitive endoscopic treatments fail, the option of surgery must be evaluated. . In patients with distal duct obstruction, calcifications, or local complications, surgery is superior to endoscopic treatment. Patients should undergo surgery early in the course of the disease to prevent further deterioration of exocrine or endocrine function. Pancreatic pseudocysts may be treated endoscopically. If endoscopic treatment fails, a surgical drainage procedure is recommended.
- This procedure was recognized as a dangerous approach, however, with lower success rates for amelioration of pain, indicating that a stenosis at the papilla of Vater is not the cause of pain in CP. resection of the tail of the pancreas, followed by a longitudinal incision of the pancreatic duct along the body of the pancreas and an anastomosis with a Roux-en-Y loop of jejunum. The modification by Partington and Rochelle abandons the resection of the pancreatic tail. these procedures are only promising if the duct is substantially dilated (>7 mm), which is the case in about 25% of all cases, and in patients who do not show a dominant mass in the head of the pancreas
- Parington-Rochelle Modification of Puestow Procedure- Lateral Pancreatico-jejonostomy
- less radical and organ-sparing procedure designed specifically for patients with CP and an inflammatory mass in the head of the pancreas Duodenumpreserving pancreatic head resection: Beger procedure. The pancreas is dissected on the level of the portal vein. The pancreatic head is excavated, and the duodenum is preserved with a thin layer of pancreatic tissue. If the bile duct is obstructed, it can be opened, and an internal anastomosis with the excavated pancreatic head can be performed (not shown). The reconstruction is performed with a Roux-en-Y jejunal loop including two anastomoses, one to the pancreatic tail remnant and one to the excavated pancreatic head. The standard reconstruction consists of a pancreaticojejunostomy to the pancreatic corpus and a side-to-side pancretoduodenectomy to the remnant of the pancreatic head by using a Roux-en-Y loop of proximal jejunum. In about 10% of patients, the DPPHR procedure is combined with lateral pancreaticojejunostomy as a consequence of multiple stenosis of the pancreatic main duct Transection of pancreatic neck—subtotal resection of pancreatic head is done, preserving the cbd and duodenum--------reconstruction is done by anastomosis of head rim and distal pancrease to the same roux limb
- Duodenum-preserving pancreatic head resection: Frey procedure. The Frey procedure combines a circumscript excision in the pancreatic head with longitudinal dissection of the pancreatic duct toward the tail. Reconstruction is performed with an anastomosis to a Roux-en-Y jejunal loop. Compared with the Beger procedure, the extent of pancreatic head resection is less; however, reconstruction is easier because it only requires one anastomosis to the pancreas. This procedure appears advantageous in patients with less severe inflammation in the head of the pancreas that is combined with an obstruction in the left-sided pancreatic duct. Head coring with longitudinal dichotomy of MPD and lateral side to side roux en Y PJ
- Duodenum-preserving pancreatic head resection: Bern modification. The Bern modif ication is a technical simplification of the Beger procedure. The extent of resection of the pancreatic head is comparable to the Beger procedure. However, the pancreas is not dissected on the level of the portal vein. Thus reconstruction can be performed with one single anastomosis of the pancreas to a Roux-en-Y jejunal loop. The bile duct may be opened if necessary, with an internal anastomosis to the loop (as demonstrated). The pancreatic duct toward the tail has to be probed to rule out distal stenosis. the pancreas is not divided at the level of the portal vein, which is often difficult because of inflammation and portal hypertension. In patients with portal hypertension and cavernous transformation of the portal vein, the risk of intraoperative bleeding is reduced by this modification Only head coring is done without dichotomy of with roux limb of jejunuim sewed to residual pancreatic head rim
- Local resection and lateral pancreatico
- Partially purified islet produce a fairly large volume of minced digested islet cell tissue which is then injected into a portal vein very slowly. But portal pressure is markedly raised several fold. Let preparation technique (Hinshaw et al)—5 ml tissue pellet is produced containing 500,000-2000,000 islets for transplantation, portal pressure remained essentially unchanged.
- Izbicki V-shaped ventral pancreatic excision. In this procedure, a long V-shaped excision of ventral aspect of the pancreas is done with a lateral pancreaticojejunostomy by a mucosa to capsule anastomosis. This procedure drains the main as well as the second and third order ducts. This is an ideal procedure for small duct disease with a maximum diameter of the Wirsung’s duct less than 3 mm.