Acute Pancreatitis

By Wichien Sirithanaphol

Definition & Incidence

An inflammatory disease of the pancreas Associated with little or no fibrosis of the gland 300,000 cases occur in the United States each year
10 to 20% = severe Leading to over 3000 deaths each year

Etiology
80 to 90 percent of the cases

Biliary tract disease

Bile duct stones (choledocholithiasis) The mechanism = not entirely clear
Common-channel hypothesis
Blockage below the junction of the biliary and pancreatic ducts Cause bile to flow into the pancreas Damaged by the detergent action of bile salts

Reflux of duodenal juice

Passage of a gallstone through the sphincter of Oddi Incompetent of sphincter

Alcohol
Consumed alcohol for at least 2 years Induce pancreatitis by several methods
The "secretion with blockage" mechanism Spasm of the sphincter of Oddi

Metabolic toxin to pancreatic acinar cells Interfere with enzyme synthesis and secretion
Increases ductal permeability Enzymes to leak out of the pancreatic duct

Transiently decreases pancreatic blood flow Focal ischemic injury to the gland

Tumor
Periampullary tumor A nonalcoholic patient No demonstrable biliary tract disease 1 to 2% of patients with acute pancreatitis
Blockage of secreted juice

Iatrogenic Pancreatitis
ERCP
- Most common - 2 to 10% of patients - Direct injury and/or intraductal hypertension

Operation that closed to the pancreas

- Pancreatic biopsy - Biliary duct exploration - Distal gastrectomy - Splenectomy

Billroth II gastrectomy
- Increased intraduodenal pressure - Backflow of activated enzymes into the pancreas

Surgery that employs low systemic perfusion

- Cardiopulmonary bypass

- Cardiac transplantation

Drugs

Infection
Mumps Coxsackie virus Mycoplasma pneumoniae

Hyperlipidemia
Lipase can liberate large amounts of toxic fatty acids into the pancreatic microcirculation - Endothelial injury
- Sludging of blood cells - Ischemic states

Miscellaneous causes
Hypercalcemic states
- Hypersecretion and the formation of calcified stones intraductally

Parasite infest ration

- Ascaris lumbricoides - Clonorchis sinensis

Hereditary pancreatitis
- Mutations in their cationic trypsinogen gene PRSS1

Azotemia
Vasculitis The sting of the Trinidadian scorpion
- Tityus trinitatis

Pathophysiology
Activation of digestive zymogens inside acinar cells Acinar cell injury Severity of the pancreatitis determined by the events that occur to acinar cell injury Mild pancreatitis
- Interstitial edema - Infiltration of inflammatory cells - little necrosis

Severe pancreatitis
- Extensive necrosis - Thrombosis of intrapancreatic vessels - Vascular disruption - Intraparenchymal hemorrhage

Symptoms
Abdominal pain
- Located in the epigastrium - Knifelike and radiating straight through to the mid-central back - May also involve both upper quadrants, the lower abdomen, or the lower chest - May have a pleuritic component and be felt in one or both shoulders - Usually abrupt in onset and slowly increases in magnitude to reach a maximal level - Usually constant pain - may be relieved by leaning forward or lying on the side with the knees drawn upward

Nausea and vomiting - May lead to gastroesophageal tears (Mallory-Weiss syndrome) and UGIB

Physical Findings
Appear ill and anxious Rolling or moving around in search of a more comfortable position Hyperthermia is common ---- Release of proinflammatory factors Tachycardia, tachypnea, and hypotension ----Hypovolemia
Diminish breath sounds in the lower lung ---- Pleuritic and abdominal pain Pleural effusion ---- More commonly the left side Jaundice ---- Distal bile duct obstruction

Abdomen ---- Ileus , localized or diffuse , epigastric mass Severe pancreatitis

- Acute lung injury
- ARDS - Retroperitoneal hemorrhage Flank ecchymoses (Grey Turner's sign) Periumbilical ecchymoses (Cullen's sign)

Amylase Measurement
Not parallel the severity of the attack Rise 2 to 12 hours after the onset of symptoms Decline 3 to 6 days after the onset of an attack Persist beyond a week suggest
- Ongoing inflammation - Development of a complication

Urinary amylase levels remain elevated longer than serum amylase Hyperamylasemia Acute cholecystitis
Perforated viscus Bowel obstruction Bowel infarction

Serum amylase activity may be normal The early stages of an attack

Overwhelming necrosis of the gland Little residual and functional pancreatic exocrine tissue Hyperlipidemia-induced pancreatitis
- be masked by circulating amylase inhibitors

Other blood tests

Lipase
- Increase usually parallels the rise in amylase activity - May persist even after amylase activity has returned to normal

Other pancreatic enzymes

- Trypsinogen
- Phospholipase - Elastase - Chymotrypsinogen

Acute phase reactants

- Interleukin -1, 6 - Tumor necrosis factor-a - C-reactive protein

Chest X-ray
Basal atelectasis Elevation of the diaphragm Pleural effusions Common on the left

Plain abdomen
Paralytic ileus Retroperitoneal gas bubbles Indicating infection with gas-forming organisms Pancreatic calcification Pathognomonic of chronic pancreatitis

Ultrasound
Extrapancreatic ductal dilations Pancreatic edema, swelling Peripancreatic fluid collections Best way to confirm the presence of gallstones in suspected biliary pancreatitis Bowel gas may obscure sonographic imaging of the pancreas

CT scan
Helpful in the diagnosis and management Pancreatic swelling and edema Pancreatic necrosis Peripancreatic or intrapancreatic fluid collections Detect and follow pseudocysts Permit fine-needle aspiration of areas suspected pancreatic infection

MRI
Same sensitivity and specificity as CT in pancreatitis

Ranson's Prognostic Signs

Mortality rates
Less than 2 signs -- generally 0% 3-5 signs --- 10 to 20% More than 7 signs --- 50%

CT severity index

Treatment of acute attack

Initial Treatment
- Diagnosis , estimating its severity, major symptoms and limiting its progression

- Severe pancreatitis are treated in an intensive care setting

Management of Pain - Most patients require narcotic medications - Meperidine are probably preferable to morphine

Fluid and Electrolyte Management

- Aggressive fluid and electrolyte repletion - Swan-Ganz or central venous pressure catheter

Nasogastric Decompression
Nutrition support - TPN or Enteral nutrition through a jejunal tube

Treatment of acute attack

Role of Prophylactic Antibiotics
- Favorably affect the course of severe pancreatitis

- No benefit to patients with mild pancreatitis - Imipenem , Imipenem with cilastatin and cefuroxime

Role of Early Endoscope and Stone Extraction

- Mild pancreatitis may require endoscopic duct clearance to prevent recurrent attacks

- Rarely benefit from early endoscopy because generally resolves spontaneously within several days - Severe biliary pancreatitis is more controversial

Treatment of acute attack

Role and Timing of Cholecystectomy in Patients With Gallstone Pancreatitis
- Intervention as soon as possible after resolution of their attack

Gallbladder-derived problems

Related to stones in the biliary ductal system

cholecystectomy

endoscopic stone clearance combined with endoscopic sphincterotomy

Treatments of Limited or Unproven Value

Peritoneal dialysis - Recent, prospective, randomized multi-institutional study --- No benefit
Reduce gastrointestinal or pancreatic secretion - H2 blockers, PPI, antacids, atropine, somatostatin, glucagon, calcitonin - Not been shown to be beneficial Anti-inflammatory agents - Steroids, prostaglandins, and indomethacin - Not been helpful Agents that inhibit activated proteolytic enzymes - Aprotinin, gabexate mesylate

- Failed to alter the course of pancreatitis - Unless their use is begun before the onset of the attack

Treatments of Limited or Unproven Value

Hypothermia, thoracic duct drainage, and plasmapheresis - In experimental models
Anti-PAF agents - Failed to show beneficially - Not currently used

Complication

1.Acute Fluid Collections

Early stages of severe pancreatitis 30 50% of patients Most are peripancreatic some are intrapancreatic More than half regress spontaneously Not regress may evolve into pseudocysts
or involve areas of necrosis

Management Sterile acute fluid collections usually resolve spontaneously No specific treatment is indicated Attempts to drain acute fluid collections --- usually unnecessary

2.Pancreatic Pseudocyst
Collections of pancreatic juice 4 to 6 weeks after the onset of an attack Usually round or oval in shape , rich in digestive enzymes Nonepithelialized wall composed of fibrous and granulation tissue Intrapancreatic or Extrapancreatic (more common) May be colonized by microorganisms --- Infected pseudocyst --- Pancreatic abscess Leakage or rupture into the peritoneal --- Pancreatic ascites Erosion into the pleural space --- Pancreaticopleural fistula Erode into a neighboring vessel --- Pseudoaneurysm and UGIB Large pseudocysts (>6 cm in diameter) - More likely to become symptomatic --- tender or mass effect Those that compress

Pancreatic Pseudocyst

Management Many pseudocysts can resolve without complications

Intervention is not mandatory in all cases unless - Symptomatic - Enlarging - Associated with complications
Methods - Excision --- distal pancreatectomy - Percutaneous catheter drainage - Internal drainage
Endoscopically --- Transpapillary drainage, cystogastrostomy, cystoduodenostomy Surgically --- Cystogastrostomy, cystoduodenostomy, Roux-en-Y cystojejunostomy

3.Pancreatic and Peripancreatic Necrosis

Areas of nonviable pancreatic or peripancreatic tissue Sterile or infected Typically include areas of fat necrosis Puttylike or pastelike consistency

4.Pancreatic Abscess and Infected Pancreatic Necrosis

Usually in proximity to the pancreas

Management

Sterile pancreatic or peripancreatic necrosis - Surgical intervention --- controversy Aggressive dbridement Nonoperative treatment

Infected necrosis - Simple antibiotic therapy ---- inadequate - Require some form of intervention - Goal of operation ---- remove as much as possible of the infected necrosis

Thank You