Acute pancreatitis


Published on

Published in: Health & Medicine, Lifestyle
1 Comment
No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide
  • In animal flow of bile to pancreatic duct not result in pancreatitis
  • transit time through sphincter, sphincterotomy not routine cause pancreatitis
  • Colocalization In normal pancreatitis , zymogen and inactive enz found in discrete organelle
  • C-reactive protein (CRP) is one of the acute phase reactants made by the liver in response to interleukin-1 and interleukin-6. Its utility for predicting the severity of pancreatitis has been studied at admission and at 24, 48, and 72 hours. A review of the literature estimated that at 48 hours, it had a sensitivity, specificity, positive predictive value, and negative predictive value of 80, 76, 67, and 86 percent, respectively, using a cutoff of 150 mg/L [ 9 ]
  • A benefit of enteral nutrition is its ability to maintain the intestinal barrier and prevent bacterial translocation from the gut, which may be a major cause of infection
  • The ACG guidelines do not recommend. if used, should be restricted to patients with pancreatic necrosis (>30 %) and continue no more than 14 d. Guidelines from the Italian Association  recommend antibiotics for patients with CT-proven necrosis
  • A, Mild acute pancreatitis showing normal enhancement of the body of pancreas after intravenous contrast. B, Severe acute pancreatitis showing pancreatic necrosis with areas of the pancreas not enhancing after IV contrast compared with areas that are normal C, Pseudocyst of the pancreas with clear-appearing fluid within the collection near the pancreas. D, Pancreatic abscess with presence of gas inside the cavity. E, Pancreatic necrosis (necrotic collection), which appears on CT scan as a clear fluid collection The same collection on MRI shows areas of necrotic debris (black arrowhead) not observed on CT scan
  • Pic 1 Arrows show peripancreatic stranding.
  • Series of 75 patients. Surgery was undertaken only for significant abdominal pain, complications, or progressive enlargement of a cyst. 52% underwent surgery for these indications, while the remaining patients were followed conservatively. Among patients in the latter group, 60% had complete resolution at one year, and only one had a pseudocyst-related complication
  • in one series of 52 patients, the mean duration of drainage was 42 days
  • Acute pancreatitis

    1. 1. Acute PancreatitisMethas Arunnart MD.Songkhla hospital
    2. 2. Anatomy
    3. 3. Introduction• Water & Electrolyte SecretionBicarbonate – most importantNa, K, Cl, Ca, Zn, PO4, SO4• Enzyme SecretionAmylolytic (amylase)Lipolytic (lipase, phospholipase A, cholesterolesterase)Proteolytic (endopeptidase, exopeptidase,elastase)Zymogen or inactive precursorsEnterokinase (duodenum) cleavestrypsinogen to trypsin
    4. 4. Etiology
    5. 5. Gallstone pancreatitis• Mechanism is not entirely clear• Common-channel theory“Blockage below junction of biliary andpancreatic duct cause bile flow intopancrease”BUT…– short channel that stone located wouldblock both biliary and pancreatic duct–Hydrostatic pressure in biliary<pancreaticduct
    6. 6. Another proposed mechanism• Gallstone through sphincter of Oddirenders it incompetent. – QuestionableBUT…–transit time through sphincter??–sphincterotomy not routine causepancreatitis
    7. 7. Mechanism???• Ductal hypertension– Cause rupture of small ducts andleakage of pancreatic juice– pH in pancreatic tissue ↓– activation of protease– “Colocalization”
    8. 8. Alcoholic pancreatitis• Common in pt. alcohol drinking > 2yr.• Often much longer upto 10 yr.• Sphincter spasm• Decrease pancreatic blood flow
    9. 9. AGA Institute
    10. 10. Diagnosis
    11. 11. Diagnostic criteriaTwo of following three features•Upper abd. pain of acute onset oftenradiating to back•Serum amylase or lipase > 3times normal•Finding on cross sectional abd. imagingReference : 2012 revision of atlanta classification of acute pancreatits
    12. 12. Physical exam•Grey Turner’s Sign- ecchymosis in 1 or both flanks•Cullen’s sign- ecchymosis in periumbilical area•Associated with Necrotizing pancreatitis• poor prognosis occurs in 1% of cases
    13. 13. Grey Turner’s Sign
    14. 14. Cullen’s Sign
    15. 15. Serum markers
    16. 16. Serum amylase• Elevates within HOURS and can remainelevated for 3-5 days• High specificity when level >3x normal• Many false positives (see next slide)• Most specific = pancreatic isoamylase(fractionated amylase)
    17. 17. Urine amylase• urinary levels may be more sensitivethan serum levels.• Urinary amylase levels usually remainelevated for several days after serumlevels have returned to normal.
    18. 18. Serum lipase• The preferred test for diagnosis• Begins to increase 4-8H after onset ofsymptoms and peaks at 24H• Remains elevated for days• Sensitivity 86-100% and Specificity 60-99%• >3X normal S&S ~100%
    19. 19. Slide 189
    20. 20. Plain Abdominal Radiograph
    21. 21. Plain Abdominal Radiograph• Bowel ileus• “Sentinel Loop”• “Colon cut off sign”• Loss of psoas shadow• Helps exclude other causes ofabdominal pain: bowel obstruction andperforation
    22. 22. Sentinel Loop•- localized ileus from nearby inflammation
    23. 23. Colon cutoff sign
    24. 24. Radiologic Findings• Plain radiographs contribute little• Ultrasound may show the pancreas inonly 25-50%• CT scan provides better information–Severity and prognosis–Exclusion of other diseases• EUS & MRI with MRCP – cause ofpancreatitis
    25. 25. Assessment of severity
    26. 26. Classification of severity- Mild : lack of organ failure andcomplications- Moderate : transient organ failureand/or complications < 48hr- Severe : persistent organ failure andcomplicationsReference : 2012 revision of atlanta classification of acute pancreatits
    27. 27. Complication
    28. 28. Early prognostic sign• Ranson’s score• APACHE II
    29. 29. Ranson’s Criteria (GB Pancreatitis)• At AdmissionAge > 70 yrWBC > 18,000/mm3Blood glucose > 220 mg/dLSerum lactate dehydrogenase > 400IU/LSerum aspartate aminotransferase >250IU/L• During Initial 48 hrHematocrit decrease of > 10%BUN increase of >2 mg/dLSerum calcium <8mg/dLArterial pO2 NASerum base deficit > 5 mEq/LioFluid sequestration > 4L
    30. 30. APACHE II• Measure at during the first 24 hoursafter admission• Using a cutoff of ≥8• The American GastroenterologicalAssociation (AGA) recommends:Prediction of severe disease by theAPACHE II system
    31. 31. APACHE II
    32. 32. Biochemical marker• CRP at 48hr– cutoff 150mg/L– Sens. 80%– Spec. 76%• TAP• Interleukins• ???
    33. 33.  CT severity scoreGrading based upon findings on unenhanced CTGrade Findings ScoreA Normal pancreas –without peripancreatic enhancement 0B Focal or diffuse enlargement of the pancreas,enhancement may be inhomogeneous on peripancreatic1C Peripancreatic inflammation with intrinsic pancreaticabnormalities2D Intrapancreatic or extrapancreatic fluid collections 3E Two or more large collections of gas in the pancreas orretroperitoneum4Necrosis score based upon contrast enhanced CTNecrosis, percent Score0 0<33 233-50 4≥50 6≥6 = severe disease.
    34. 34. Treatment
    35. 35. Treatment• General Considerations- adequate IV hydration and analgesia- NPO- NG tube: not routinely used* But may be used in patients with ileus or intractable N/V• Nutrition• Early enteral feeding• Nasojejunal tube feeding• PPN,TPN
    36. 36. Nutrition• Used high protein, low fat, semi-elemental feeding (eg, Peptamen AF)because reduced pancreatic digestiveenzymes.• Start at 25 cc/hr and advanced to atleast 30% of daily requirement(25 kcal/kg IBW)
    37. 37. Nutrition• Signs that the formula is nottolerated include- gastric residual volumes >400 cc- vomiting (with nasogastric feeding)- bloating- diarrhea (>5 watery stools or >500 mL/d)
    38. 38. Treatment• Metabolic Complications- Correction of electrolyte imbalance - Ca,Mg- Cautiously for hyperglycemia• Cardiovascular Care• Respiratory Care• Deep vein thrombosis prophylaxis
    39. 39. Prophylactic antibiotics–Although this is still an area of debate–Not indicated for mild attack–suggest imipenem or meropenemfor 14 days for patients with provennecrosis
    40. 40. TREATMENT OFASSOCIATED CONDITIONS• Gallstone pancreatitis– ERCP should be performed within 72hours in those with a high suspicion ofpersistent bile duct stones– EUS & MRCP should be considered in casethat clinical is not improving sufficiently– Cholecystectomy +/- IOC
    41. 41. Cholecystectomy??• should be performed after recovery in allpatient with gallstone pancreatitis• Failure to perform a cholecystectomyis associated with a 25-30% risk of recurrentacute pancreatitis, cholecystitis, or cholangitiswithin 6-18 weeks
    42. 42. Cholecystectomy• In mild pancreatitis case, an usually beperformed safely within 7 days after recovery• In severe pancreatitis case ,delaying for atleast 3 wks may be reasonable• If high suspicion of CBD stones, preoperativeERCP is the best test that therapeuticintervention will be required• If low suspicion,intraoperative cholangiogramduring cholecystectomy may be preferable toavoid the morbidity associated with ERCP
    43. 43. Complication
    44. 44. Local Complications• Pseudocyst• Abscess• Necrosis–Sterile–InfectedMild pancreatitis severe pancreatitisPseudocyst abscessPancreatic necrosis
    45. 45. New Classification Based onContrast-Enhanced CT (CECT)*• Interstitial Edematous Pancreatitis–Acute Peripancreatic Fluid Collection–Pancreatic Pseudocyst• Necrotizing Pancreatitis–Acute Necrotic Collection–Walled-Off Necrosis
    46. 46. Interstitial Edematous VS Necrotizing• Interstitial Edematous Pancreatitis– Pancreatic parenchyma enhances with thecontrast agent– Lack of peripancreatic necrosis• Necrotizing Pancreatitis– Pancreatic parenchymal areas without IVcontrast enhancement +/- Peripancreaticnecrosis (see below—ANC and WON)
    47. 47. Interstitial Edematous VS Necrotizing
    48. 48. Acute Peripancreatic FluidCollection (APFC):Occurring within the first 4 weeks in thesetting of interstitial edematous pancreatitis.• CECT Criteria–Homogeneous fluid adjacent to pancreasconfined by peripancreatic fascial planes–No recognizable wall
    49. 49. Pancreatic Pseudocyst• An encapsulated, well-defined collection offluid but no or minimal solid components• Occurs >4 weeks after onset of in interstitialedematous pancreatitis• CECT Criteria– Well-defined wall , homogeneous, roundor oval fluid collection– No solid component– Only in interstitial edematous pancreatitis
    50. 50. APFC vs Pseudocyst
    51. 51. Acute Necrotic Collection(ANC)• A collection of both fluid and solidcomponents (necrosis) occurring duringnecrotizing pancreatitis.• This collection can involve the pancreaticand/or the peripancreatic tissues• CECT Criteria– Heterogeneous– No encapsulating wall– Intrapancreatic and/or extrapancreatic
    52. 52. Walled-Off Necrosis(WON)• A mature, encapsulated ANC with a well-defined inflammatory wall• these tend to mature >4 weeks after onset ofnecrotizing pancreatitis.• CECT Criteria– Heterogenous– Well-defined wall– Intrapancreatic and/or extrapancreatic
    53. 53. ANC vs WON
    54. 54. Infected pancreatic necrosis.• The most common organisms include E.coli,Pseudomonas, Klebsiella, and Enterococcus
    55. 55. Guideline management ofsevere pancreatitis
    56. 56. AGA Guideline
    57. 57. Surgical debridement
    58. 58. Management of pseudocyst
    59. 59. Management of pseudocyst• Watchful waiting:- Operative intervention was recommendedfollowing an observation period of 6 wks- However, there are some reports supportmore conservative approach
    60. 60. Management of pseudocyst• Surgical drainage – gold standardOpen vs endoscopic–cystgastrostomy–Cystenterostomy–Cystojejunostomy, Cystoduodenostomy–Ressection
    61. 61. Management of pseudocyst• Percutaneous catheter drainage– As effective as surgery in draining and closing bothsterile and infected pseudocysts– Catheter drainage is continued until the flow ratefalls to 5-10 mL/day– If no reduction in flow, octreotide(50 -200 µg SC q 8hr) may be helpful.– Should follow-up CT scan when the flow rate isreduced to ensure that the catheter is still in thepseudocyst cavity– more likely to be successful in patientswithout duct-cyst communication
    62. 62. Management of localcomplication of pancreatitis
    63. 63. Indication forpancreatic debridement• Infected pancreatic necrosis• Symptomatic sterile pancreatic necrosis• chronic low grade fever• Nausea• Lethargy• Inability to eat• * Fail medical treatment
    64. 64. Timing of debridement• The optimal timing is at least 3-4wksfollowing the onset of acute pancreatitis.• Delayed debridement allows– clinical stabilization of the patient– resolution of early organ failure– decreased inflammatory reaction, andnecrotic areas are demarcated
    65. 65. Surgical approach• Open debridement with external drainage– gold standard• Open debridement with internal drainage andcystgastrostomy- only appropriate for patients with WON• Open packing— Open packing with planned reoperation every48-72 hrs until the necrosis is adequately removed• Laparoscopic debridement-Video-assisted retroperitoneal debridement-Laparoscopically-assisted transperitonealdebridement