chronic pancreatitis anoop k r

PANCREATITIS

HISTORY

• 24 Y

• Female

• 30th Oct 2012

HISTORY

• Pain upper abdomen – 2 years

EXAMINATION

• Young lady sitting in bed, well oriented in time place and person.

• Vitals:

• Pulse = 80/min

• B.P = 110/70 mmHg

• R.R = 16/min

• Temp = A/F

EXAMINATION

• Abdomen:

• Soft

• Mildly tender epigastrium

• BS = +ve

EXAMINATION

• Chest:

• NAD

• CVS

• NAD

• CNS

• NAD

INVESTIGATIONS

• Labs

• WNL

USG ABDOMEN (2010)

• Dilated pancreatic duct with stone at junction of head and body of pancreas.

ERCP (2010)

• Large stone which cannot be retrieved.

• Papillotomy performed.

USG ABDOMEN (2012)

• Pancreas is scarred.

• Dilated pancreatic duct.

• Large stone measuring 16 x 20 mm is noted in the pancreatic duct at the junction of pancreatic head and body.

COMPUTERIZED TOMOGRAPHY

• Dilated pancreatic duct with proximal narrowing.

• Large intraductal calculus at the junction of head and body.

• Panrenchymal thickening in the region of head and body.

• Peripancreatic fat stranding.

• Pancreatic tail is normal.

MANAGEMENT

• Pain relief

• Lateral pancreaticojejunostomy

POST OP

• Recovery was smooth.

• Patient was pain free.

CHRONIC PANCREATITIS

CHRONIC PANCREATITIS

• Permanent and irreversible damage to the pancreas, with histologic evidence of chronic inflammation, fibrosis, and destruction of exocrine (acinar cell) and endocrine (islets of Langerhans) tissue.

EPIDEMIOLOGY

FREQUENCY

• In US = 87,000 cases/year

GENDER

• Males are affected more than females (6.7 vs 3.2 cases/100,000)

• Alcohol-induced illness is more prevalent in males.

• Idiopathic and hyperlipidemia-induced pancreatitis is more prevalent in females.

• Equal sex ratios are observed in hereditary pancreatitis.

AGE

• Mean age at diagnosis is 46 ± 13 years

RACE

• Blacks are affected more than whites.

PATHOPHYSIOLOGY

INTRADUCTAL PLUGGING AND OBSTRUCTION

• Alcohol abuse

• Stones

• Tumors

TOXINS AND TOXIC METABOLITES

• Act on acinar cells cytokines release stellate cells stimulation fibrosis

• Oxidative stress• Alcohol

• Smoking

• Necrosis-fibrosis

• Ischemia• Important exacerbating factor

• Autoimmune disorders• Sjögren syndrome

• Primary biliary cirrhosis

• Renal tubular acidosis.

EITIOLOGY

METABOLIC

• Excessive alcohol consumption

• Most common cause.

• 60-70% of chronic pancreatitis cases are due to alcohol consumption but only 10-15% alcoholics develop the disease.

• Increases protein secretion and decreased fluid and bicarb production.

• Viscous protenaceous debris becomes insipissated within the lumen, causing ductular obstruction.

METABOLIC

• Hyperlipidemia

• Usually presents with repeated attacks of acute pancreatitis.

• Hypercalcemia

• Now a rare cause

• Nutritional or tropical chronic pancreatitis

GENETIC

• Hereditary pancreatitis

• Autosomal dominant

• Cystic fibrosis

IDIOPATHIC CHRONIC PANCREATITIS

• Approximately 20 % of cases.

OBSTRUCTION

• Congenital abnormalities

• Pancrease divisum

• Acquired obstruction

• Blunt abdominal trauma

• Stones

• tumors

AUTOIMMUNE PANCREATITIS

• Uncommon, less than 1% cases

• Diffuse enlargement of pancreas

• Diffuse and irregular narrowing of the main pancreatic duct

• Increased circulating levels of IgG4

• Autoantibodies

• Association with other autoimmune disease.

ETIOLOGY

• Alcohol 70%

• Idiopathic (including tropical) 20%

• Other 10%• Hereditary

• Hyperparathyroidism

• Hypertriglyceridemia

• Autoimmune pancreatitis

• Obstruction

• Trauma

• Pancrease divisum

Schwartz’s Principles of Surgery 8th ed

PANCREATIC STONES

• Calcium carbonate crystals trapped in a matrix of fibrillar and other material.

• The fibrillar center of most stones contains no calcium, but a mixture of other metals.

• Stones form from an initial noncalcified protein precipitate (PSP/lithostathine), which serves as a focus for layered calcium carbonate precipitation.

• PSP/lithostathine are potent inhibitors of CaCO3 crystal growth.

• Availability fo PSP/lithostathine in duct fluid of alcoholic patients is decreased by elevated levels of precipitation and decreased production. increased CaCO3 crystal deposition.

FIBROSIS

• A common feature of all forms of chronic pancreatitis is the perilobular fibrosis that forms surrounding individual acini, then propagates to surround small lobules, and eventually coalesces to replace larger areas of acinar tissue.

• The sentinel acute pancreatitis event (SAPE) hypothesis

PRESENTATION

SYMPTOMS AND SIGNS

• Abdominal pain

• Most common symptom.

• Located in epigastrium

• Penetrating through to back

• Steady and boring

• Exacerbated by eating and drinking

• Nausea and vomiting

• Malabsorption

• Occurs when pancreatic exocrine capacity fall below 10% of normal.

• Weight loss

• Diarrhea

• Steatorrhea

• Pancreatogenic (Brittle) Diabetes

• Acinar tissue loss and replacement by fibrosis is greater than the degree of loss of islet tissue.

• Frank diabetes is seen initially in about 20% of patients with chronic pancreatitis, and impaired glucose metabolism can be detected in up to 70% of patients.

• Ketoacidosis and diabetic nephropathy are relatively uncommon in pancreatogenic diabetes

• Pancreatogenic (Brittle) Diabetes

• Global deficiency of all three glucoregulatory islet cell hormones: insulin, glucagon, and pancreatic polypeptide (PP).

• The expression of the hepatic insulin receptor gene, and the subsequent availability and action of insulin receptors on hepatocyte membranes, are regulated by PP.

• Paradoxical combination of enhanced peripheral sensitivity to insulin, and decreased hepatic sensitivity to insulin.

Parameter Type I IDDM Type II NIDDM Type III Pancreaticogenic

Ketoacidosis Common Rare Rare

Hyperglycemia Severe Usually mild Mild

Hypoglycemia Common Rare Common

Peripheral insulin sensitivity

Normal or increased Decreased Increased

Hepatic insulin sensitivity Normal Normal or Decreased

Decreased

Insulin levels Low High Low

Glucagon levels Normal or high Normal or high Low

Pancreatic polypeptide levels

High High Low

Typical age of onset Childhood or adolescence

Adulthood Any

TESTS FOR CHRONIC PANCREATITIS• Measurement of pancreatic products in blood

• Enzymes• Pancreatic polypeptide

• Measurement of pancreatic exocrine secretion• Direct measurements

• Enzymes• Bicarb

• Indirect measurements

• Bentiromide test• Schilling test• Fecal fat• [14C]-olein absorption

• Imaging techniques• Palin radiograph abdomen• Ultrasonography• Computed tomography• Endoscopic reterograde cholangiopancreatograhy• Magnetic resonance cholangiopancreatography• Endoscopic ultrasonography

Endoscopic Ultrasound Features of Chronic PancreatitisEndoscopic Ultrasound Feature Implication

Ductal changesDuct size >3 mm Ductal dilationTortuous pancreatic duct Ductal irregularityIntraductal echogenic foci Stones or calcificationEchogenic duct wall Ductal fibrosisSide-branch ectasia Periductal fibrosis

Parenchymal changesInhomogeneous echo pattern EdemaReduced echogenic foci (1–3 mm) EdemaEnhanced echogenic foci CalcificationsProminent interlobular septae FibrosisLobular outer gland margin Fibrosis, glandular atrophyLarge, echo-poor cavities (>5 mm) Pseudocyst

COMPLICATIONS

PSEUDOCYST

• A chronic collection of pancreatic fluid surrounded by a nonepithelialized wall of granulation tissue and fibrosis.

• The most common complication of chronic pancreatitis.

• Pseudocysts are multiple in 17% of patients.

• Pseudocysts communicate with the pancreatic ductal system in up to 80% of cases.

• They may occur intrapancreatically, or extend beyond the region of the pancreas into other cavities or compartments.

• Usually cause symptoms of pain, fullness, or early satiety.

Definitions of Pancreatic Fluid Collections

Term DefinitionPeripancreatic fluid collection A collection of enzyme-rich pancreatic juice which occurs early in the course of

acute pancreatitis, or which forms after a pancreatic duct leak; located in or near the pancreas, it lacks a well organized wall of granulation or fibrous tissue

Early pancreatic (sterile) necrosis

A focal or diffuse area of nonviable pancreatic parenchyma, typically occupying more than 30% of the gland, and containing liquefied debris and fluid

Late pancreatic (sterile) necrosis An organized collection of sterile necrotic debris and fluid with a well-defined margin or wall within the normal domain of the pancreas

Acute pseudocyst A collection of pancreatic juice enclosed within a perimeter of early granulation tissue, usually as a consequence of acute pancreatitis which has occurred within the preceding 3–4 weeks

Chronic pseudocyst A collection of pancreatic fluid surrounded by a wall of normal granulation and fibrous tissue, usually persisting for more than 6 weeks

Pancreatic abscess Any of the above in which gross purulence (pus) is present, with bacterial or fungal organisms documented to be present

PSEUDOCYST

• Asymptomatic pseudocysts can be managed expectantly, and may resolve spontaneously or persist without complication.

• Symptomatic or enlarging pseudocysts require treatment.

• The management of a pseudocyst should involve the multidisciplinary approach for evaluation and selection of any given treatment strategy.

PSEUDOCYST

• If infection is suspected, the pseudocyst should be aspirated (not drained) by CT- or US-guided fine-needle aspiration, and the contents examined.

• If infection is present, and the contents resemble pus, external drainage is employed using either surgical or percutaneous techniques.

PSEUDOCYST

• If the pseudocyst has failed to resolve with conservative therapy and symptoms persist, internal drainage is usually preferred to external drainage.

• Percutaneous catheter based method

• Endoscopic method

• Surgical method

• Transpapillary duct drainage method

PANCREATIC ASCITES

• Disrupted pancreatic duct leads to pancreatic fluid extravasation that does not become sequestered as a pseudocyst, but drains freely into the peritoneal cavity.

• The pancreatic fluid tracks superiorly into the thorax, and a pancreatic pleural effusion occurs.

• Pancreatic ascites and pleural effusion occur together in 14% of patients.

• Paracentesis or thoracentesis reveals noninfected fluid with a protein level greater than 25 g/L and a markedly elevated amylase level.

PANCREATIC ASCITES

• ERCP is most helpful to delineate the location of the pancreatic duct leak.

• Antisecretory therapy with the somatostatin analog octreotide acetate, together with bowel rest and parenteral nutrition, is successful in more than half of patients.

• Reapposition of serosal surfaces to facilitate closure of the leak is considered a part of therapy.

• A period of chest tube drainage may facilitate closure of the internal fistula.

• Surgical therapy is reserved for those who fail to respond to medical treatment.

PANCREATIC-ENTERIC FISTULA

• The most common site of communication is the transverse colon or splenic flexure.

• Presents with evidence of gastrointestinal or colonic bleeding and sepsis.

• When the fistula involves the colon, operative correction is usually required.

HEAD-OF-PANCREAS MASS

• An inflammatory mass develops in head of pancreas in upto 30% of patients.

• Commonly presents with severe pain.

• Duodenum preserving pancreatic head resection.

SPLENIC AND PORTAL VEIN THROMBOSIS

• Splenic vein thrombosis occurs in association with chronic pancreatitis in 4 to 8% of cases.

• Portal vein compression and occlusion can occur as a consequence of an inflammatory mass in the head of the pancreas.

• Variceal formation.

• The mortality risk of bleeding exceeds 20%.

• The addition of splenectomy to prevent variceal hemorrhage is prudent when surgery is otherwise indicated to correct other problems.

TREATMENT

MEDICAL THERAPY

• Analgesia

• Alcohol abstention

• Oral analgesics are prescribed alone or with analgesia-enhancing agents such as gabapentin.

• Use of narcotics should be titrated to achieve pain relief with the lowest effective dose.

MEDICAL THERAPY

• Enzyme Therapy

• Reverses the effects of pancreatic exocrine insufficiency.

• Non-enteric coated preparations reduce enteric signals for pancreatic enzymes secretion reduce intraductalpressure reduce pain.

• Enteric coated preparations result in little to no pain relief.

• Enteric coated preparations are treatment of choice for steatorrhea.

MEDICAL THERAPY

• Antisecretory Therapy

• Somatostatin administration has been shown to inhibit pancreatic exocrine secretion and CCK release.

• Severe pain exacerbations in chronic pancreatitis can benefit from a combination of octreotide therapy and TPN.

MEDICAL THERAPY

• Neurolytic Therapy

• the use of radiologically- or endoscopically-guided celiac plexus blockade in chronic pancreatitis has been disappointing.

ENDOSCOPIC MANAGEMENT

• Pancreatic duct stenting is used for treatment of proximal pancreatic duct stenosis, decompression of a pancreatic duct leak, and for drainage of pancreatic pseudocysts that can be catheterized through the main pancreatic duct.

• Minor papilla sphincterotomy and dorsal duct stenting for chronic pancreatitis due to pancreas divisum.

• Idiopathic pancreatitis patients have been treated with endoscopic stenting, pancreatic duct sphincterotomy, and endoscopic stone removal.

• Extracorporeal shock wave lithotripsy (ESWL) has been used for pancreatic duct stones, together with endoscopic stenting and stone removal.

SURGICAL THERAPY

HISTORY OF SURGICAL THERAPY

• 1911 – Pancreatostomy by Link.

• 1942 – Total pancreatectomy by Priestley.

• 1946 – Proximal pancreatic resection by Whipple.

• 1940 – 1950 – Sphincteroplasty.

• 1954 – Roux en Y pancreaticojejunostomy by Duval and Zollinger.

• 1958 – Roux en Y lateral pancreaticojejunostomy by Puestow and Gilllesby.

• 1960 – Roux en Y lateral pancreaticojejunostomy by Partington and Rochelle.

• 1980 – Duodenal preserving pancreatic head resection by Begger.

• 1987 – Local resection of pancreatic head with longitudinal pancreaticojejunostomy by Frey and Smith

SPHINCTEROPLASTY

• Endoscopic sphincteroplasty

• Transduodenal sphincteroplasty.

DRAINAGE PROCEDURES

• The effectiveness of decompression of the pancreatic duct is dependent on the extent to which ductal hypertension is the etiologic agent for the disease.

• Successful pain relief after the Puestow-type decompression procedure has been reported in 75 to 85% of patients for the first few years after surgery, but pain recurs in >20% of patients after 5 years.

• The surgical management of pancreatic duct stones and stenosis has been shown to be superior to endoscopic treatment in randomized clinical trials in which the long, side-to-side technique of pancreaticojejunostomy is used.

Duval caudal pancreaticojejunostomy

Peustow and Gillesby’s longitudical pancreaticojejunostomy

Puestow Procedure

RESECTIONAL PROCEDURES

DISTAL PANCREATECTOMY

• For patients with focal inflammatory changes localized to the body and tail, or in whom no significant ductal dilatation exists, the technique of partial (40 to 80%) distal pancreatectomy has been advocated.

• Distal pancreatectomy is less morbid than more extensive resectional procedures.

• Long-term outcomes reveal good pain relief in only 60% of patients, with completion pancreatectomyrequired for pain relief in 13% of patients.

NINETY-FIVE PERCENT DISTAL PANCREATECTOMY

• Pain relief in 60 to 77% of patients long term.

• High risk of brittle diabetes, hypoglycemic coma, and malnutrition.

PROXIMAL PANCREATECTOMY

• Proximal pancreatectomy or pancreaticoduodenectomy, with or without pylorus preservation has been widely used for the treatment of chronic pancreatitis.

• Pain relief 4 to 6 years after operation was found in 71 to 89% of patients.

• Mortality ranged from 1.5 to 3%.

• In follow-up, 25 to 48% of patients developed diabetes.

TOTAL PANCREATECTOMY

• This operation produces no better pain relief for their patients than pancreaticoduodenectomy (about 80% to 85%).

• The metabolic consequences are profound and life-threatening.

DPPHR

• Pain relief maintained in 91% after 6 years follow up.

• Mortality <1%.

• Diabetes 21%.

• Similar complication risk as in the Whipple procedure.

LR-LPJ

• Excavation of the pancreatic head including the ductal structures in continuity with a long dichotomy of the dorsal duct.

• Preservation of the pancreatic neck as well as the capsule of the posterior pancreatic head.

• Pain relief in 87% of patients.

• No operative mortality

• Postop complications 22%.

DENERVATION PROCEDURES

• Symptomatic relief in patients with persistent and disabling pain who are poor candidates for resection or drainage procedures.

• Neurolytic therapy

• celiac ganglionectomy or splanchnicectomy

• Transhiatal splanchnicectomy

• Transthoracic splanchnicectomy with or without vagotomy

• Videoscopic transthoracic splanchnicectomy.