Acute pancreatitis

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Acute pancreatitis

  1. 1. ACUTE PANCREATITIS DR.BARUN KUMAR
  2. 2. At a glance • Etiology • Pathogenesis • Diagnostic assessment
  3. 3. DEFINITIONS • An acute inflammatory process of pancreas that may also involve peripancreatic tissue or remote organ system • Requires 2 out of following 3 features: 1. Abdominal pain characteristic of acute pancreatitis 2. Serum amylase and/or lipase level >/ 3 times the upper limit of normal 3. Characteristic findings of acute pancreatitis on ultrasonography or CT scan
  4. 4. ETIOLOGY • Alcohol • Gallstone • Post-ERCP • Drugs • Autoimmune • Genetic • Abdominal trauma • Post operative • Infections • Metabolic - hypercalcemia, hyperparathyroidism, hypertriglyceridemia • Miscellaneous- scorpion bite, worm infestations
  5. 5. A.ALCOHAL • Along with gallstone, alcohol is the major etiological agent of acute pancreatitis • Heavy ethanol abuse >100g/day for at least 5 years, smoking and genetic predisposition bears strong risk for alcohol induced injury. • Alcohol has both direct(caspases ,sphincter of oddi obst,dec perfusion) and indirect (nf-kb, tnf-alpha, IL-1) effects on exocrine pancreas • N34S , SPINK-1 mutation association
  6. 6. B.GALLSTONE • Responsible for as many as 40% of cases, especially in northern belts of india and woman aged 50-70 years. • OBSTRUCTIVE THEORY: excessive pressure inside the pancreatic duct due to obstruction and subsequent activation of enzymatic and inflammatory cascade • REFLUX THEORY: stones impacted in ampulla of vater resulting in reflux of bile in pancreatic duct.
  7. 7. C.POST-ERCP • Occurs in as high as upto 5% of patients • Most common complication of ERCP • More common in therapeutic ERCP than diagnostic • Major risk factors include use of precut sphincterotomy, number of pancreatic duct cannulation, and duct opacification. • 2 theories have been proposed: a)Traumatic intubatiuon of ampulla causing sphincter spasm b)Excessive hydrostatic pressure during contrast injection causing acinar cell damage
  8. 8. D.MICROLITHOIASIS : association with idiopathic recurrent acute pancreatitis E.GENETICS : IRAP and idiopathic chronic pancreatitis shows strong genetic association PRSS1 (cationic trypsinogen gene) , SPINK1 (42% association) , CFTR (9% association) F. HYPERTRIGLYCERIDEMIA: a level of >1000 mg/dl is suggestive >2000 mg/dl is diagnostic G.CONGENITAL ANAMOLIES: pancreas divisum needs modifiers or cofactors
  9. 9. H. DRUG INDUCED PANCREATITIS: I. HYPERSENSITIVITY : 5-aminosalicyclic acid, azathioprine, 6-mercaptopurine,metronidazole, tetracycline II.DURG INDUCED HYPERTRIGLYCERIDEMIA: thiazide, isotretinoin, tamoxifen III. TOXIC METABOLITE: pentamidine, valproic acid, didanosine IV. OVERDOSE REACTION: acetaminophen, erythromycin
  10. 10. I. INFECTIONS: hep A , HEP B (well recognised) HEP C, HEV mumps, EBV,VZ,CMV J. ASCARIASIS: KASHMIR is the most affected area with as high as 23% cases of acute pancreatitis due to ascariasis K. HYPERPARATHYROIDISM: the primary mechanism is calcium mediated activation of trypsinogen or calcium depostion in pancreatic duct
  11. 11. L. AUTO-IMMUNE PANCREATITIS: • auto immune infiltration of pancreas lymphoplasmacytic cells resulting in focal or diffuse enlargement of pancreas. • However, there is no features of pancreatitis. Instead there are features of obstructive jaundice. • Serum IgG4 levels > 1400 mg/l OR IgG4 positive cells in IHC
  12. 12. PATHOGENESIS • The exact mechanism and detailed understanding is still unknown. • However, most researchers believe abnormal activation of pancreatic enzymes inside the pancreatic acinar cells is the basic pathology • This further leads to immune response which then is responsible for both local changes and systemic response
  13. 13. FIG. pathophysiology of acute pancreatitis
  14. 14. MAJOR STEPS IN PATHOPHYSIOLOGY : A.INTRA-ACINAR EVENTS B. INNATE IMMUNE RESPONSE C. MICROCIRCULATORY DISTURBANCES D.BACTERIAL INFECTIONS
  15. 15. A. INTRA – ACINAR EVENTS The key event is intra pancreatic activation of the digestive enzymes either through : i. Ach mediated vagal stimulation ii. Enterokinase activation under pH dependant reaction iii. Trypsin is the first enzyme to get activated which then in turn activates other enzymes Protecting factors: i. SPINK 1 : packing of inactive intracellular enzymes away from proteolytic enzymes ii. Low intracellular pH- prevents trypsin activation iii. Maintenance of particulate subcellular Ca gradient COLOCALIZATION THEORY: colocalization of zymogen granules and lysosomes in presence of increased cytosolic Ca gradient
  16. 16. B. INNATE IMMUNE RESPONSE : Activation of vascular adhesion molecules Attraction of neutrophils neutrophil elastase mediated injury ( measured by MPO) Monocyte mediated injury (through IL-1, IL-6 and TNF-alpha) Results in damage and further inactivation and the cycle continues (Levels of TNF-alpha and IL-6 correlates with the degree of severe pancreatitis )
  17. 17. C. MICROCIRCULATORY DISTURBANCE Leucocyte adhesion, hemoconcentration and vasoconstriction Reduced capillary perfusion and ischemia Further pancreatic injury Pancreatic necrosis Effects on systemic circulation with circulatory failure, hypotension and acute renal failure
  18. 18. D. BACTERIAL INFECTION The necrosed pancreatic tissue and peripancreatic fluid collection are susceptible sites for bacterial infection The most common source of infection is gut through transmigration of bacteria Most common organsim : E.Coli , pseudomonas, klebsiella Infected pancreatic necrosis carries a high mortality of as high as 40% Institution of early enteral feeding is instrumental of preventing transmigration of bacteria
  19. 19. DIAGNOSTIC ASSESSMENT A. CLINICAL DIAGNOSIS B.LABOROTORY DIAGNOSIS C. ASSESSMENT OF SEVERITY
  20. 20. Clinical Presentation • Pain (95%) – Acute onset – Mid-abdominal or mid-epigastric – Radiates to the back (50%) – Peak intensity in 30 minutes – Lasts for several hours • Nausea and vomiting (80%) • Fever • Shock • Abdominal distension (75%) • Abdominal guarding and tenderness (50%) • Restlessness and agitation • Grey-Turner's sign (hemorrhagic discoloration of the flanks) • Cullen's sign (hemorrhagic discoloration of the umbilicus)
  21. 21. Cullen's sign Grey-Turner's sign
  22. 22. LABORATORY DIAGNOSIS • Serum amylase : alone cannot be used reliably for the diagnosis of AP and serum lipase is preferred. • Serum lipase is more specific and remains elevated longer than amylase after disease presentation. • Increased amylase and/or lipase >3 times – Amylase levels rise w/in 2-12h • Peak w/in first 48hr • Remain elevated 3-5days before return to baseline – Lipase much more specific
  23. 23. .• Abdominal ultrasound US should be performed in all patients with AP • In the absence of gallstones and / or history of significant history of alcohol use, a serum triglyceride should be obtained and considered the etiology if >1000 mg/dl • In a patient > 40 years old, a pancreatic tumor should be considered as a possible cause of AP
  24. 24. CT SCAN/ MRI • CT/MRI is the modality of choice for diagnosis and evaluation and diagnosis of acute pancreatitis • However, patients with mild acute pancreatitis need not undergo ct/mri • CT/MRI is indicated when: 1. Clinical diagnosis is doubtful 2. Failure to respond to medical management in 48-72 hrs 3. Any change in clinical status suggestive of complication CT/MRI offers the advantage of evaluation of extent and severity of disease
  25. 25. MDCT PROTOCOL FOR ACUTE PANCREATITIS 60 SEC DELAY Dome of diaphragm to symphysis pubis PORTAL VENOUS PHASE 35 SEC DELAY COVERAGE THROUGH PANCREAS TO LOOK FOR NECROSIS PANCREATIC PARENCHYMAL PHASE 10 SEC DELAY Top of the vertetbral body T12 to sup edge of L4 (in suspected vascular complications) Arterial phase CONTRAST – 150 ml of 60% iodinated non-ioinc iv @3-4 ml/sec
  26. 26. MODIFIED CT SEVERITY INDEX PROGNOSTIC INDICATOR POINTS PANCREATIC INFLAMMATION • NORMAL PANCREAS • INTRINSIC PANCREATIC ABNORMALITIES WITH/WITHOUT INFLAMMATORY CHANGES IN PERIPANCREATIC FAT 0 2 • PANCREATIC OR PERIPANCREATIC FLUID COLLECTION OR PERIPANCREATIC FAT NECROSIS 4 PANCREATIC NECROSIS • NONE 0 • <30% 2 • >=30% 4 EXTRAPANCREATIC COMPLICATIONS one or more of pleural effusion, ascites , vascular complications, parenchymal complications, or gastrointestinal tract involvement 2
  27. 27. . • Higher CTSI score associated with protracted clinical course, a higher complication rate and a higher mortality • CTSI 0-1 = no morbidity or mortality • CTSI 2 = morbidity rate of 4% and no mortality • CTSI 7-10% = 17% mortality and 92% complication rate
  28. 28. CT Findings Tail Indistinct Intraperitoneal fluid
  29. 29. CT Findings Severe Pancreatitis Nonenhancin g Necrosis Peripancreatic edema and inflammation
  30. 30. CLINIAL ASSESSMENT HISTORY PLUS EXAMINATIONS SYMPTOMPS OUT OF PROPORTION THAN SIGNS SERUM AMYLASE + SERUM LIPASE USG W/A CT SCAN / MRI ASSESSEMENT OF RISK
  31. 31. RISK ASSESSMENT A. ATLANTA SCORING
  32. 32. ATLANTA CRITERIA ( CONTD.) CHARACTERISTICS DEFINING POINT ORGAN FAILURE SHOCK (SBP <90mm of Hg) Pulmonary insufficiency (PaO2<60 mm oh Hg) Renal failure (serum creatinine level >2mg/dl after rehydration) Gastrointestinal bleeding (>500 mL/24 hr) LOCAL COMPLICATIONS PANCREATIC NECROSIS (>30% of the parenchyma or >3 cm) PANCREATIC ABSCESS ( circumscribed collection of pus containing little or no pancreatic necrosis) PANCREATIC PSEUDOCYST (collection of pancreatic juices enclosed by a wall of fibrous tissue or granulation tissue) UNFAVOURABLE PROGNOSTIC SIGNS RANSONS SCORE >=3 APACHE II SCORE >=8
  33. 33. ATLANTA CRITERIA ( CONTD.) CHARACTERISTIC DEFINING POINT SYSTEMIC COMPLICATIONS DIC (platelet count <100000) FIBRINOGEN (1GR/L FIBRIN SPLIT PRODUCTS >80 ug/dl METABOLIC DISTURBANCE ( calcium level <7.5 mg/dl)
  34. 34. B.RANSON SCORE At admission • age in years > 55 years • white blood cell count > 16000 cells/mm3 • blood glucose > 11 mmol/L (> 200 mg/dL) • serum AST > 250 IU/L • serum LDH > 350 IU/L At 48 hours • Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL) • Hematocrit fall > 10% (as compared with admission value) • Oxygen (hypoxemia PO2 < 60 mmHg) • BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration • Base deficit (negative base excess) > 4 mEq/L • Sequestration of fluids > 6 L
  35. 35. C.APACHE-II SCORE • ACUTE PHYSIOLOGY AND CHRONIC HEALTH EVALUATION • predicts severity of any acute disease • consists of 11 parameters reflecting functions of major organ system also taking age amd baseline chronic disease into account • allow for monitoring of disease progression and response to therapy • Has been shown superior to ranson and glasgow
  36. 36. I.MARSHALL SCORING SYSTEM ORGAN SYSTEM 0 1 2 3 4 RESPIRATORY (P02/FiO2) >400 301-400 201-300 101- 200 <=100 RENAL Serum creatinine, mg/dl <1.4 1.4-1.8 1.9-3.6 3.6-4.9 >4.9 CARDIOVASCULAR Systolic blood pressure, mm oh Hg >90 <90 Fluid responsive <90 Not fluid responsive <90 pH<7.3 <90 pH<7.2
  37. 37. . D. SIRS SCORE • hr>90/min, • TEMP >38 or <36 celcius • Resp rate >20 breaths/min or PaCO2>32 mm oh Hg • Blood cell count >12000 or <4000 cells/microlit or >10% band form E. BISAP SCORE o BUN> 25 mg/Dl o Impaired mental status (gcs<15) o SIRS >=2 o Age>60 yrs o Pleural effusion
  38. 38. .F. Panc 3 score • Hemotocrit >44 , bmi>30kg/m2, pleural effusion G.JAPANESE SEVERITY SCORE • Has 9 components • Score of 3 or more reflects severe acute pancreatitis H. HARMLESS ACUTE PANCREATITIS SCORE • Absence of rebound tenderness and/or guarding • Normal hematocrit • Normal serum creatinine  Enables scoring within 30 mins of admn  In a cohort of 394 patients, has shown the accuracy to predict a mild course of acute pancreatitis as high as 98%
  39. 39. BIOCHEMICAL PREDICTORS OF PANCREATIC NECROSIS AND SEVERITY 1. C-reactive protein (CRP) - >150 mg/ml 2. Proclcitonin (PCT) 3. Serum amyloid –a (SAA) 4. Serum macrophage migration inhibitory factor (MIF) 5. Trypsionogen activation peptide (TAP) 6. Polymorphonuclear granulocyte elastase (PMN) 7. Interleukin 8. Hematocrit 9. Bun
  40. 40. THANK YOU • ,

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