Pancreatitis

ACUTE PANCREATITIS

ETIOLOGY Acute Pancreatitis             

                                      

Abuse of ethanol Biliary tract stones Drugs Endoscopic Retrogradecholangiopancreatography Hypercalcemia Hyperlipidemia Idiopathic Infections Ischemia Parasites Postoperative Scorpion sting (Tityus trinitatis ) Trauma

 Chronic Pancreatitis

      

   Autoimmune    Duct obstruction    Ethanol abuse   Hereditary   Hypercalcemia   Hyperlipidemia    Idiopathic

Cullen’s sign

Grey-turners’s sign

CRP  C-reactive protein  A C-reactive protein (CRP) value can be

obtained 24-48 hours after presentation to provide some indication of prognosis. Higher levels have been shown to correlate with a propensity toward organ failure.  A CRP value in double figures (ie, >10 mg/dL) strongly indicates severe pancreatitis. CRP is an acute-phase reactant that is not specific for pancreatitis.  The sensitivity of this test is 73%, and the

Prognostic markers  Trypsin activation peptide (urine)  Polymorphonuclear elastase  Interleukin-6  Phospholipase A2 

B

carboxypeptidase

 Serum amyloid A  Procalcitonin

RANSON’S CRITERIA

DRAW BACKS  First, 11 criteria are used, some of which

are evaluated on day 1 and others on day 2. The Ranson score is valid only at 48 hours after onset and not at any other time during the disease.  Second, the threshold for an abnormal value depends on whether the pancreatitis is caused by alcohol or gallstones.  Finally, the sensitivity is only 73% and the specificity is 77% to predict morality

IMRIE’S GLASGOW SYSTEM 1. Age >55 years 2. White blood cell count >15,000/mm3 (15.0 X 109/L) 3. Blood glucose >180 mg/dL (10 mmol/L) in patients without diabetes 4. Serum lactate dehydrogenase >600 U/L 5. Serum AST or ALT >100 U/L 6. Serum calcium <8 mg/dL 7. PaO2 <60 mm Hg 8. Serum albumin <3.2 g/dL (32 g/L) 9. Serum urea >45 mg/dL (16.0 mmol/L) Scoring: One point for each criterion met 48 hours after admission [>3 Factors means severe]

ATLANTA DEFINITIONS  ACUTE: acute inflammatory process of

pancreas with variable involvement of other tissues/organ systems.  MILD ACUTE : minimal organ

dysfunction and uneventful recovery.(interstitial edema of pancreas)  SEVERE ACUTE: MODS / local

complication

BALTHAZAR CT GRADING OF SEVERITY

Necrosis score: None (0 points) >one third (2 points) one half (6 points) Using the Balthazar criteria ,the sensitivity is 87%, and the specificity CT INDEX: CT grade + is SEVERITY 88%. necrosis score

 CT-guided needle aspiration  This procedure is used to differentiate infected

necrosis and sterile necrosis in patients with severe necrotizing pancreatitis.  The needle is placed into an area of low attenuation in or around the pancreas of a patient with fever and tachycardia or other signs of a systemic inflammatory response syndrome, generally following the first week of severe pancreatitis. The procedure may be repeated weekly if clinically indicated.  The specimen should be delivered to the laboratory within an hour and interpreted promptly. The specimen should always be evaluated for Gram stain, culture, and sensitivity.  If the Gram stain shows bacteria or fungi, surgical debridement of the infected necrosis is generally indicated. An exception would be if the patient could not tolerate surgery; in this case, CT-guided

Early treatment  Aims of treatment are to :  To halt progression of local disease  Prevent remote organ failure

 Requires full supportive therapy – often In

ICU  Urinary catheter, CVP line and possibly arterial line  Regular assessment of U+Es, Ca, blood sugar, LFTs  Patients require:  Fluid resuscitation with both colloid and

crystalloid  Correction of hypoxia with an increased inspired oxygen or ventilation  Adequate analgesia - opiate or epidural

Nutritional support  Pancreatitis is associated with a    

catabolic state The benefit of pancreatic 'rest' by limiting oral intake is unproven Evidence that early enteral nutrition is safe Nasojejunal feeding limits pancreatic secretion Preferable to oral or nasogastric feeding

SURGICAL TREATMENT  INDICATIONS:

2. Infected pancreatic necrosis. 3. Sterile necrosis not responding to conservative management. 4. Persistent necrotising pancreatitis 5. Fulminant acute pancreatitis 6. Complications (bleeding/bowel perforation)

TIMING OF SURGERY  As late as possible  Rationale – easy to differentiate

between well demarcated necrotic and viable tissue.  > 4 weeks after onset of symptoms.  Early surgery only in proven infested necrosis or complications.

TECHNIQUES  Conventional Approach     Débridement with reoperation when clinically 

      

indicated or at planned intervals    Débridement with open or closed packing and reoperation when clinically indicated or at planned intervals    Débridement with continuous lavage Unconventional Approach    Antibiotics alone    Antibiotics with percutaneous drainage    Antibiotics with endoscopic drainage    Antibiotics with surgical drainage but not débridement    Antibiotics with débridement through minimally invasive surgery

 Emerging treatments  Although the role cytokines play in systemic

inflammatory response syndrome appears important, a recent large clinical trial of lexipafant, a platelet-activating factor antagonist, has shown no benefit in patients with severe acute pancreatitis.  Because multiple pathways are involved in the inflammatory response, further research is needed in order to define which cytokine or combination of cytokines should be targeted to ameliorate the complications of acute pancreatitis.  Anti-tumor necrosis factor-alpha therapy has recently been targeted as a potential

1.    Acute Fluid Collections. These occur during the early stages of severe pancreatitis in 30% to 50% of patients, they lack a wall of granulation or fibrous tissue, and more than half regress spontaneously. Most are peripancreatic, but some are intrapancreatic. Those that do not regress may evolve into pseudocysts or involve areas of necrosis. 2.    Pancreatic and Peripancreatic Necrosis. These are areas of nonviable pancreatic or peripancreatic tissue that may be either sterile or infected. They typically include areas of fat necrosis, and the necrotic tissue has a puttylike or pastelike consistency. Some necrotic regions may evolve into pseudocysts, whereas others may be replaced by fibrous tissue

 Pancreatic Pseudocyst. These are collections of

pancreatic juice, usually rich in digestive enzymes, that are enclosed by a nonepithelialized wall composed of fibrous and granulation tissue  Pancreatic Abscess and Infected Pancreatic

Necrosis. These are circumscribed intraabdominal collections of pus, usually in proximity to the pancreas, which contain little or no necrotic tissue but arise as a consequence of pancreatitis