Acute pancreatitis final

acute pancreatitis

1. ACUTE PANCREATITIS By: Dr .NANDHINI

2. ETIOLOGY GALL STONES (30% - 60%) ALCOHOL(15% - 30%) POST ERCP (5% - 10%) POST TRAUMATIC (1%) DRUGS POST OPERATIVE

3. DRUGS 1.Azathioprine 8.Dapsone 2. 6MP 9.INH 3.Asparginase 10.Metronidazole 4.Pentamidine 11. estrogens 5.Didanosine 12.Tamoxifen 6.Valproate 13.Corticosteroids 7.Tetracyclines 14.ACE (-) tors 15. Thiazides

4. Contd … Vascular causes & Vasculitis CTD Carcinoma head of pancreas Infections Bacterial: mycoplasma , MAC, Campylobactor , leigionella , Lptospirosis . Viral: Mumps,Rubella,Varicella , Coxsackie , CMV,echo virus. Parasites: Ascaris , Clonorchis )

5. Contd … Auto immune (type 1&2) Scorpion bite Malnutrition Peritoneal dialysis etc….

6. If recurrent episodes……. Metabolic : hypertriglyceridemia , hypercalcaemia Pancreatic divisum IPMN Heriditary Pancreatitis Cystic fibrosis Drugs Idiopathic

7. PATHOGENESIS MOST ACEPTED THEORY --- AUTO DIGESTION PHASES 1. Enzyme Autoactivation 2.Chemoattraction & sequestration ofPMN and macrophages releasing CK 3. Local & Systemic effects

8. TRYPSIN Other Proenzyme activation Autoactivation Prophospholipase Pro elastase prekallikrein Phospholipase elastase kallikrein Fat necrosis weakens BV clotting . cascade HEMORRHAGE

9. Others…… Genetic : 1. PRSS1 (cationic trypsinogen gene) 2.SPINK1 (pancreatic secretory trypsin inhibitor) 3.CFTR 4.CTRC ( chymotrypsin receptor gene) 5.CASR (calcium sensing receptor gene) Hypertriglyceridaemia Hypercalcaemia Drugs

10. Enzyme activation mechanisms Pancreatic duct obstruction Primary acinar cell injury Defective intracellular transport of Enzymes Leucocyte sequestration Releases chemokines like IL-1ß ,IL-6, TNF, PAF, SubstanceP . Sustains injury Local and sytemic effects

11. CLINICAL PRESENTATION

12. Epigastric pain (D/D) Nausea,Vomiting Abdominal distension Cool perpheries Blindness (may be transient) Respiratory distress Hiccoughs

13. Mild Icterus Signs of shock SIRS Cullens sign Grey turners sign Fox sign Erythematous tender skin nodules Evidence of pleural effusion Guarding and rigidity Sluggish bowel sounds

14. Fox sign

15. Mechanism

16. Other obsolete signs : Korte sign Kamenchick sign Mayo robsons sign

17. DIAGNOSIS 2 of these 3criteria Typical abdominal pain 3 fold or more raise in serum Amylase or Lipase CT findings s/o accute Pancreatitis

18. REVISED ATLANTA CLASSIFICATION

19. ACUTE PANCREATITIS Interstitial Necrotising Acute peripancreatic Acute Necrotic Fluid collection Collection after 4wks Pseudocyst Walled of Necrosis

20. MORPHOLOGICAL FEATURES 1. INTERSTITIAL PANCREATITIS No necrosis Diffuse enhancement

21. 2.ACCUTE PANCREATIC FLUID COLLECTION (APFC) no necrosis Peri pancreatic fluid <4wks duration No encapsulation No intra pancreatic extension

22. 3.Pancreatic pseudocyst No necrosis >4wks duration Well encapsulated Homogenous fluid density

23. 4. ACUTE NECROTISING PANCREATITIS Parenchymal or peri pancreatic necrosis

24. 5.ANC (Acute Necrotic Colletion ) Necrotic areas Heterogenous areas Intra or peri pancreatic extension Non encapsulated

25. 6.WON(Walled Of Necrosis) Necrotic areas >4wks duration Heterogenic fluid collection Well encapsulated Intra or peri pancreatic collection

26. SEVERITY ASSESSMENT

27. Assessing injury to other organs 1. SOFA score 2. Modified Marshall Scoring System

28. Assessing severity of Pancreatitis 1. BISAP score 2.Ransons score 3. Glasgow score 4. APACHE-II score 5. CT severity Index 6. Modified CT severity Index 7.HAPS score 8.Revised Atlanta Classification

29. SOFA SCORE Assesses 6 systems i.e , respiratory cardiovascular renal hepatic coagulation neurological

30. MODIFIED MARSHALL SCORING SYSTEM

31. BISAP score B – BUN > 22mg% I - Impaired mental status S - SIRS (Any 2 of 4 criteria) A - Age >60 yrs P -Pleural effusion

32. RANSON’S score On Admission With in 48 hrs of admission WBC > 16,OOOcells/ cumm AGE >55yrs Glucose >200mg/dl LDH > 350 IU/L AST > 250U/L PCV fall > 10% Arterial Po2 < 60mm Hg BUN raise > 5mg% Calcium < 8 mg/dl Base Deficit > 4mEq/L Fluidsequestration > 6lit

33. RANSONS SCORE 11 point scoring system POINTS ------ MORTALITY 0-2 - 0% 3-4 - 15% 5-6 - 50% >6 - 70%

34. GLASGOW SCALE On admission With in 48 hrs WBC > 15,000 cells/ cumm Age > 55yrs Glucose > 200 mg/dl Arterial Po2 <60 mmHg Urea >45 mg/dl S.Calcium <8mg/dl S.Albumin <3.2mg/dl S.LDH >600U/L S.ALT > 200 U/L

35. APACHE – II scoring system 12 point scoring system After 24 hrs of admission into ICU

36. CTSI Includes BALTHAZAR SCORE & NECROSIS SCORE

37. BALTHAZAR SCORE GRADE --- DESCRIPTION --- SCORE A Normal pancreas B Enlarged pancreas 1 C Inflammatorychanges 2 in pancreas and peri pancreatic fat D Ill defined single 3 peripancreatic fluid collection E ≥2 Ill defined fluid collections 4

38. NECROSIS SCORE % --- SCORE NONE 0 ≤30% 2 30-50% 4 >50% 6

39. Grading 0-2 : Mild 4-6 : Moderate 8-10 : severe

40. HAPS (Harmless Acute Pancreatitis Score) High PPV Used to predict a milder course of illness Includes 1.Guarding &/ Rebound tenderness +/- 2.Creatinine <2mg/dl 3.Hematocrit < 43%(M) <39.6%(F) Score of “0” good prognosis

41. ATLANTA CLASSIFICATION MILD : no local complications & organ failure MODERATELY SEVERE : transient organ failure <48hrs +/- local complications SEVERE : persistent organ failure (>48hrs) with local and systemic complications

42. GRADING OF SEVERITY OF ATTACK BISAP score of 3 - 5 Ransons ’ score ≥ 3 Glassgow score ≥ 3 APACHE II score ≥ 8 CTSI (Balthazar) ≥ 6 Modified CTSI score of 8-10 Persistent organ failure( RevisedAtlanta ) CRP >150mg/dl

43. Lab parameters………. *CBP * Hematocrit * S. Amylase * BUN * S. lipase * S.Creatinine * S. Calcium * CRP * S. Triglycerides * LFT *S. Trypsin * Coagulation * Blood sugar profile

44. ENZYMES S.Amylase Normal values 23-85U/L Sources : parotids, pancreas, fallopian tube, sweat, Types : S-type and P-type ( isoenzymes ) Metabolism : renal & hepatic Half life : 7 to 14 hrs sensitive & Highly nonspecific

45. High Amylase levels seen in *Pancreatic disorders *Salivary disorders *Renal failure * Macroamylasemia *Intestinal diseases- gut infarction perforation , peritonitis,obstruction * Ruptured ectopic pregnancy * ectopic production : cancers of pancreas, thymus, breast, lung ,ovary. * DKA and other acidotic conditions

46. Amylase No corelation b/n severity of pancreatitis and degree of enzyme elevation Usually rises within 24hrs of attack and returns to normal within 48-72hrs After 3-7 days normalises even if inflammation continues. Hence normal levels doesn’t exclude the disease

47. Amylase – P more specific than serum Amylase

48. Low Amylase levels………….. May be seen in certain pancreatic cancers Toxaemia of pregnancy

49. Confirmed Pancreatitis with Normal Amylase levels….. Hypertriglyceridemia (high triglycerides interferes with enzyme assay) Some times in patients with Alcoholic pancreatitis

50. S.Lipase More specific (95%) Remains for longer time in serum than amylase Stays even upto 8to 14 days useful in patiets who are presenting lately Half life about 10to 14hrs Level of lipase can’t predict disease severity and outcome

51. High serum lipase levels seen in *Hollow viscus perforation *Intestinal obstruction *Intestinal ischemia In case of Alcoholic pancreatitis S. lipase is more elevated than S.Amylase

52. S.CALCIUM May be high or low Hypercalcemia – cause Hypocalcemia - effect of pancreatitis Low Calcium levels correlates with severity of disease <7mg/dl with normal albumin levels associated with tetany have poor prognosis

53. S. TRIGLYCERIDES High levels of >900-1000 mg/dl associated with increased risk Estimated in fasting states Usually asso . with Type I ,V Hyperlipidemias

54. Markers of Hemoconcentration *BUN > 22 mg/dl * Hematocrit atAdmission >44 %( highNPV ) * S.Creatinine at 48 hrs of Admission > 1.8mg/dl (high PPV) Helpful in assessing fluid status of patient Predictors of Pancreatic Necrosis

55. CRP Elevated CRP of >150 mg/dl at 48 hrs of admission suggestive of severe disease. single important prognostic indicator of severity LFT hyperbilirubinemia >4mg/dl may be seen in 10% patients assiciated with gall stone associated pancreatitis Elevated ALP also seen

56. IMAGING IN PANCREATITIS

57. ROLE OF PLAIN X-RAY

58. SIGNS Sentinal loop Colon cutoff sign Renal halo sign Loss of psoas shadow Gall stone may be seen Multiple calcifications in case of accute on chronic pancreatitis patient pleural effusion Lt> Rt

59. COLON CUTOFF SIGN

60. D/D for Colon Cut Off sign *Pancreatitis *IBD *Mesenteric ischemia *Carcinoma Colon

61. SENTINAL LOOP SIGN D/D

62. ROLE OF USG AND DOPPLER

63. Diffuse Decrease in Pancreatic Echogenicity (than liver) Free fluid Increased volume of Pancreas i.e , Bulky Pancreas (AP diameter >24mm) Gall stones Parenchymal inhomogenicty may correlate with necrosis Pseudocysts Spleenic vien thrombosis etc..

64. ROLE OF CT IN PANCREATITIS

65. MANAGEMENT

66. 1.FLUID RECUSCITATION Main stay of therapy Initially 15-20ml/kg bolus administered Then f/b 3ml/kg/hr infusion should be kept to maintain urine output of >0.5cc/kg/hr Serial evaluations done to assess fluid status clinically and by measuring BUN & Hematocrit every 8-12 hrs.

67. Decrease in serial BUN & Hematocrit ensues adequate resuscitation Adjust fluid rates of infusion in patients with co morbid cardiac , pulmonary , renal illnesses Increasing BUN & Hematocrit inspite of aggressive fluid therapy can be treated with repeated volume challenge with 2L crystalloid bolus f/b increase in infusion rate by 1.5ml/kg/hr .

68. If still unresponsive transfer to intensive unit for careful hemodynamic monitering . Fluid of choice is Lactated Ringer which reduces systemic inflammation and preffered over Normal Saline

69. 2. Pain Management Opiates like Buprenorphine is DOC Pethidine can be given alternatively Meperidine 100to 150mg IM can be given every 4 th hrly if necessary NSAID of choice is Metimazole Morphine is contraindicated.

70. 3.NBM NPO is no longer advisable Usually kept for 2-3 days with ryles tube aspiration As soon as possible oral fluids are allowed even enzymes are elevated Initially with soft liquids Later with low fat diet preferred Maintains barrier integrity and decreases bacterial translocation

71. 4. Role of Antibiotics Prophylactic therapy has no role Mild disease doesn’t needs antibiotics at all For severe pancreatitis i.e , with necrosis may benefit Definitive role is seen with proven cases of infected Necrosis Antibiotics of choice are CARBAPENUMS

72. IMIPENUM 5oomg 8 th hrly given Alternatively Cefuroxime 1.5g IV TID f/b 250mg oral BD for 14 days Meropenum and combination of Ciprofloxacin and Metronidazole doesn’t appear to reduce frequency of infected necrosis and MODS

73. 5.Supportive therapy FFP transfusions in case of DIC Ionotropes for cardiac support Mechanical ventilation for ARDS Hemofilteration etc….

74. In Spl situations like…… 1. Gall stone pancreatitis : *should undergo ERCP within 24-48hrs of admission to prevent recurrence * cholecystectomy may be done on later date

75. 2.Hypertriglyceridemia : *Initially treated with Insulin , Heparin, plasmapheresis * later hypolipidemic drugs like Fibrates , Niacin can be used. 3. ERCP induced Pancreatitis: *Rectal Indomethacin , Allopurinol , newer drug Ulinastatin , aggressive hydration with ringered lactate can prevent this .

76. COMPLICATIONS

77. SYSTEMIC LOCAL Pleural effusion ARDS Atelectasis Hypotension arrythmias Pericardial effusion DIC ATN Renal vein /artery thrombosis Hyperglycemia Encephalopathy Purtscher’s retinopathy Subcutaneous fat necrosis Acute fluid collection Necrosis (sterile/infected) Pseudocyts Pancreatic abscess Portal / spleenic vein thrombosis Pseudoaneurysm

78. PURTSCHER’S RETINOPATHY

79. NECROSIS May be sterile(60%) or infected(40%) Prophylactic antibiotics no role Infected necrosis can be suspected by clinical deterioration with persistant MODS Aspirated under CT guidance sent for gram’s and culture

80. Pseudocyst Emperical antibiotic therapy with Imipenum can be started Step up approach Requires 4wks for epithelisation and maturation Resolve spontaneously with in 6wks May or may not communicate with ductal system

81. SURGEON’S ROLE 1. Necrosis - necrosectomy *indications : worsening sepsis in case of infected necrosis 2.pseudocyst – >6cm lasting for 12 wks producing pressure symptoms warrants surgery

82. Prognosis Risk of chronic pancreatitis after an attack of accute alcoholic pancreatitis is 13% in 10 yrs & 16% in 20 yrs

83. Follow up care Aimed towards assessment of risk of DM Exocrine Pancreatic insufficiency etc..

84. THANK U