Acute pancreatitis ‫‬

Lectrure By:
DR.TARIK S. ALNOGOMI
ER Chief. EMERGENCY MEDICINE SPECIALIST
MEGAT GENERAL HOSPITAL

1. ACUTE PANCREATITIS DR.TARIK S. ALNOGOMI ER MEGAT GENERAL HOSPITAL

2. WHY PANCREATITIS…?

3. WHY PANCREATITIS…?

4. NOT UNCOMMON PATHOLOGY

5. SERIOUS CONDITION POTENTIALLY

6. ACUTE PANCREATITIS CAUSES BILIARY ALCOHOLIC IDIOPATHIC

7. OTHER UNUSUALL CAUSES HYPERLIPIDEMIA HYPERCALCEMIA CONGENITAL VIRAL DRUGS TRAUMATIC OTHER CAUSES

8. Trans-abdominal ultrasound should be performed in ALL patient with acute pancreatitis to assess gallstones as etiology of acute pancreatitis. In absence of gallstones or significant alcohol use, obtain serum triglycerides . If serum triglycerides > 1,000 mg/ dL , consider as etiology of acute pancreatitis. In patients > 40 years of age, consider pancreatic tumor in absence of other causes. In patients < 30 years of age and +FH of acute pancreatitis in absence of other causes, consider genetic testing for hereditary pancreatitis. Etiology

9. PATHOLOGY OSTRUCTION - SECREATION COMMON CHANNEL THEORY DUODENAL REFLUX INCREASED PANCREATIC DUCT PERMEABILITY . ENZYME AUTOACTIVATION

10. Acute Pancreatitis - Pathophysiology Premature Activation of Trypsin → Autodigestion of pancreatic tissue ACTIVATION OF INFLAMMATORY RESPONSE Inflammatory mediators Vasodilation SHOCK ARDS MODS ATN 10 Extravascular movement of serum albumin 3 rd spacing Panc. edema SHOCK

11. 11

12. ACUTE OEDEMATOUS PANCREATITIS ACUTE PERSISTENT UNRESOLVING . ACUTE NECROTIZING , FULMINANT . RECURRENT ACUTE PANCREATITIS

13. ACUTE PANCREATITIS IN INFANTS AND CHILDRENS …???

14. PRESENTATION OF ACUTE PANCREATITIS ABDOMINAL PAIN NAUSEA VOMITING RETCHING HYPOTENTION

15. SIGNES OF ACUTE PANCREATITIS FINDING OF ABD. EXAMINATION CULLEN , S SIGNE GREY TURNER , S SIGNE later FINDING OF COMPLICATIONS

16. Pain, Oh the pain “Worse than childbirth” “Worse than being shot” Starts fast within 10-20min reaches peak Third fastest pain onset in GI after perf and SMA thromb Does not usually undulate (not colicy) Lasts days (if no underlying chronic damage) Longer than biliary colic which is hours Radiate to back in 50% Sometimes diagnosed at autopsy (painless) Almost always causes ER visit/admission Capsaicin, glutamate, vanilloid, ppar-gamma

17. ECG CHANGES ……???

18. Acute Pancreatitis 20 40 60 80 100 Presenting features Abdominal pain Nausea / vomiting Tachycardia Low grade fever Abdominal guarding Loss of bowel sounds Jaundice

19. 80%

20. 20%

21. UPPER ABDOMINAL PAIN CLINICAL PRESENTATION Tiger Land ....!! Lord .. Zakhary Cope

22. ???????????????

23. DIAGNOSIS

24. SCIENTIFIC BASE !

25. CLINICAL SENCE

26. HISTORTY .. !!

27. PROPER EXAMINATION

28. INVESTIGATIONS

29. DIFFERANTIOAL DIAGNOSIS ? REFERED PAIN FROM THE CHEST ABDOMINAL CAUSES

30. INFERIOR MYOCARDIAL INFARCTION

31. PERFORATED PEPTIC ULCER

32. UPPER INTESTINAL OBSTRUCTION

33. MESENTERIC VASCULAR OCCLUSION

34. acute cholecystitis

35. Surgical Abdomen .. !!!

36. جل من لايسهو ... جل من لايخطئ

37. LAPORATORY INVESTIGATION CBC UREA CREATININE RBS SERUM ELECTROLYTES LFT SERUM AMYLASE

38. AMYLASE

39. IS THERE OTHER CAUSES FOR ELEVATED SERUM AMYLASE….?

40. OTHER INVESTIGATIONS URINARY AMYLASE : CREATININE CLEARANCE RATIO. TIMED URINARY AMYLASE OUTPUT AMYLASE CLEARANCE STUDIES SERM LIPASE IN NECROTISING PANCREATITIS COMPLEMENT C3 AND C4 (INCREASE) ALPHA2 MACROGLOBULIN (DECRAESES) ALPHA2 PROTEASES (DECREASES)

41. Acute Pancreatitis: Time course of enzyme elevations Hours after onset Fold increase over normal 6 12 24 48 72 96 2 4 6 8 10 12 Lipase Amylase Amylase half life 10 hrs

42. TO WHAT LEVEL IS DIAGNOSTIC….?

43. Serum A mylase (25-125 U/L)  >200 U/L for 24-72 hours starts to rise 2-6 hr after onset of pain Peaks @ 24 hours Return to normal @ 72 hr Serum Lipase (3-19 U/ dL ) used with amylase; rises later than amylase (48 hours) return to normal 5-7 days  WBC’s  glucose  lipids  calcium  magnesium

44. Blood tests Amylase and lipase Plasma level peak within 24 hours t 1/2 of amylase << lipase Sensitivity Specificity Amylase 67-100 85-98 Lipase 82-100 86-100 Gut 1997,41:431-35; Br J Surg 1998,84:1665-69.

45. IN ACUTE PANCREATITIS IS SERUM AMYLASE ALWAYS HIGHT……???

46. CXR ABDOMINAL XRS ERECT SUPINE

47. ABDOMINAL ULTRASOUND WHAT IS THE ROLE OF ABD US IN ACUTE PANCREATITIS ……?? DIAGNOSTIC …..!!? FOLLOW UP …!!?

48. ABDOMINAL CT SCAN DIAGNOSTIC …!!? FOLLOW UP…!!? WHAT TYPE …!!?

49. CT Scan Normal Homogeneous enhancement of the whole pancreas Abnormal Non-visualization of a part of the pancreas Sensitivity of 90-95% Specificity – 100%

50. CT scan Not necessary for the diagnosis Diagnostic doubt Atypical presentations Asymptomatic hyperamylasaemia or hyperlipasemia Gastroenterol Clin N Am 1990;19:811-42

51. Recommendation A dynamic CT scan should be performed in all (predicted) severe cases between 3 and 10 days after admission (Evidence grade B)

52. http://dbwmpns0f8ewg.cloudfront.net/images/a_panc/ct_apanc.jpg

53. Magnetic Resonance Cholangio-Pancreatography ( MRCP) Sensitivity of > 90%

54. Endoscopy Ultrasound (EUS) EUS Sensitivity of > 95% Specificity of > 95-100%

55. IPMN

56. Clinical indices of severity RANSON APACHE ATLANTA Balthazar score BISAP Glasgow Delta HCT and/or Delta BUN

57. Multiple Factors Scoring System Ranson Separate for alcohol and gallstone etiology Score > 3 = severe acute pancreatitis Glasgow valid in all types of pancreatitis Both of these systems require 48 hours from the admission for full assessment Can J Gastroent 2003 325-328

58. Ranson At presentation Age >55 White blood cell count >16 Blood glucose >200 mg/ dL LDH >350 U/L AST >250 U/L At 48 hours Hematocrit Fall by ≥10% BUN Increase by ≥5 mg/ dL despite fluids Serum calcium <8 mg/ dL pO2 <60 mmHg Base deficit >4 MEq /L Fluid sequestation >6 L 1-2 criteria - > <1% mortal 3-5 cirteria - > 15% mortal 6-8 criteria- > 60% mortal 9-11 -> >75% mortal .

59. APACHE II A cute P hysiology and C hronic H ealth E valuation as good as the Ranson or Glasgow at 24 and 48 hours of the admission APACHE II score > 8 = Severe acute pancreatitis Cumbersome to use if one does not use a pc or palm - where the formula is easily downloaded Br J Surg 1997,84:1665-69

60. APACHE II Temp high or low MAP high or low HR high or low (HR 60 gets 2pts!) Na high or low K high or low Creat elev Age over 44 APACHE-O BMI>25 1 pt BMI>30 2pts WBC high or low Glasgow coma (low) pH or HCo3 High or low PaO2 Nonsurgical and emergency surgery More points Score <8 Mortal <4% Score >8 8-18%

61. Grading of pancreatitis ( Balthazar score ) A: normal pancreas: 0 B: enlargement of pancreas: 1 C: inflammatory changes in pancreas and peripancreatic fat: 2 D: ill-defined single peripancreatic fluid collection : 3 E: two or more poorly defined peripancreatic fluid collections: 4 Pancreatic necrosis  none: 0 ≤30%: 2 >30-50%: 4 >50%: 6 The maximum score that can be obtained is 10. Treatment and prognosis The CTSI is the sum of the scores obtained with the Balthazar score   and those obtained with the evaluation of pancreatic necrosis: 0-3: mild acute pancreatitis 4-6: moderate acute pancreatitis 7-10: severe acute pancreatitis

62. Desirable features of Markers of Severity Accuracy - High S ensitivity Predictability within 24 hours of admission Easy to use

63. BISAP SIRS T >38.5°C or <35.0°C, HR>90, RR >20 or PaCO 2 <32 mm Hg WBC >12,000, <4000 or >10 percent immature (band) forms BUN>25 Age>60 Pleural effusion Altered mental status ( glasgow CS < 15) 0-2 pts: <2% mortal 3-5pts: 22% mortal

64. ATLANTA (1992) Mild vs severe (necrosis or organ failure) APACHE≥8 or RANSON≥3 Organ failure Systolic blood pressure <90 mmHg Pulmonary insufficiency PaO2 ≤ 60 mmHg Renal failure Creatinine ≥2 mg/dl after rehydration Gastrointestinal bleeding 500 ml in 24 h DIC: Platelets ≤100 fibrinogen <1·0 g/l and fibrin-split products >80 μ g/l Calcium ≤7·5 mg/dl

65. ATLANTA REVISED (2008) Early severity->organs fail Late severity->Structural (necrosis), esp infect PERSISTANT ORGAN FAILURE (>48 hrs) NEW DEFs of Radiographic/structural features of severity

66. Current Recommendations Mild to moderate Ranson < 3 APACHE II < 8 Severe Ranson >3 APACHE II >10 Organ failure Pancreatic necrosis

67. If a multiple factor scoring system is to be used, the best choice at present appears to be APACHE II calculated at 24 hours - Evidence category A

68. Is It Possible to Predict Severity Early in Acute Pancreatitis? Good clinical judgment Specificity - 80% Sensitivity - 40% Scoring Specificity – 60% Sensitivity – 95%

69. CRP is currently the gold standard Amylase and lipase of no value High likelihood that IL-6/ TAP will replace the CRP Recommendations

70. Advantage Used to monitor the clinical course of the disease Disadvantage Not always present on admission Lack specificity C-reactive protein (CRP)

71. C-reactive protein (CRP) Gold standard for the prediction of the necrotizing course of the disease Accuracy of 86% Readily available

72. C-reactive protein (CRP) Acute phase reactant Synthesized by the hepatocytes Synthesis is induced by the release of interleukin 1 and 6 Peak in serum is three days after the onset of pain Most popular single test severity marker used today Isenmann et al Pancreas 1993;8:358-61

73. Management of Acute Pancreatitis

74. Treatment Of Acute Pancreatitis UNCOMPLICATED PANCREATITIS …. MEDICAL SELF LIMITED IN MOST CASES AIM FLUIDS AND ELECTROLYTES PANCREATIC SECRETION

75. KEEP PATIENT …… NPO UNTILL WHEN …??? NASOGASTRIC SUCTION ……..??? AGGRESSIVE FLUIDS REPLACEMNT MANGEMENT OF HYPO. K ,Ca ,CL,Mg . OXYGEN

76. WHAT IS ABOUT…??

77. ANTICHOLINERGICS…..??? ANTIACIDES ……. ???

78. GLUCAGON ……??? SOMATOSTATIN .. ?? TRACYLOL ……. ???

79. ANTIBIOTICS …..????

80. Antibiotics Sepsis Accounts for > 80% of deaths Intestinal flora Gram negative bacteria Mechanism – translocation of the bacteria across the gut wall

81. Antibiotics - Rationale Early (1 week) Sterile necrosis Massive inflammatory response – multi-system organ failure (SIRS) Late – Infected necrosis

82. Why the controversy ? Early trials in 1970’s did not show the benefit of antibiotics Antibiotics that did not penetrated the pancreatic tissue

83. Evidence 8 clinical trials Five of these trials showed a significant reduction in the incidence of pancreatic infections 1 trial showed a significant reduction in mortality Limitations Small sample size None were double blinded randomized placebo controlled trials

84. Antibiotics ? Increased risk of fungal infections Associate with mortality as high as 85%

85. Recommendations Prophylactic antibacterial treatment is strongly recommended in severe pancreatitis (Evidence B) No evidence when to start prophylactic treatment or how long to continue therapy Appropriate antibiotics are those that are active against in particular gram-negative organisms Commence as early as possible after the identification of a severe attack

86. Therapy Treatment Antifungal therapy – definite role

87. Fungal Infection Antibiotics predispose to candida infection of the pancreatic tissue which increases the mortality substantially

88. Fungal infection 92 patients with infected pancreatic necrosis 22 patients (24%) with Candida infection Patients with Candida infections Suffered higher mortality (64% vs. 19%, p=.0001) More systemic complications Were given preoperative antibiotics for a longer period (19 vs 6 days; p=.0001) World J. Surg. 25,372-76

89. Fungal Infection Candida Torulopsis Commensal organism found in human gastrointestinal tract Incidence 10-40%

90. KEEP PATIENT …… NPO UNTILL WHEN …??? NASOGASTRIC SUCTION ……..??? AGGRESSIVE FLUIDS REPLACEMNT MANGEMENT OF HYPO. K ,Ca ,CL,Mg . OXYGEN

91. Evolution in Nutrition Fasting TPN is better Early jejunal feeding is safe Early jejunal feeding is superior Gastric feeding is as good as jejunal feeding

92. Current Recommendations Jejunal feeding should be started within 48 hours The optimal feeding formulae is unknown Ensure the jejunal placement of the tube Monitor for Hypertryglyceridemia/ hyperglycemia TPN in patients who do not tolerate enteral feeding

93. IPMN

94. ERCP AND ES INDICATION ....? WHEN …..?

95. LOCAL … GENERAL … COMPLICATIONS OF ACUTE PANCREATITIS

96. LOCAL COMPLICATIONS PANCREATIC EXTRAPANCREATIC

97. PANCREATIC PANCRATIC NECROSIS PANCREATIC INFECTION PANNCREATIC ABSCESS PANCREATIC FISTULA PANCREATIC ASCITES PSUDOCYST

98. EXTRAPANCREATIC INTRABDOMINAL HAEMORRHAGE GASTROINTESTINAL HAEMORRHAGE PORTAL VEIN THROMBOSIS BILIARY OBSTRUCTION DUODENAL OBSTRUCTION

99. Acute Pancreatitis Complications Pulmonary Cardiovascular Coagulation Renal l Immunological Pleural Effusion (enzyme induced Inflammation of Diaphragm) Atelectasis Abdominal distention &  diaphragmatic movement 3 rd spacing BP, HR Vasoconstriction d/t SNS activation Trypsin activates both clotting & lysing factors  DIC & PE Hypovolemia GFR Renal perfusion Clots in renal circulation ATN ARF GI motility bacteria outside GI Pancreatic abscess Necrosis infection 120

100. Markers of Inflammation TNF-alpha Major role in mediating inflammatory response Conflicting reports as a predictor of severity Interleukin-6 and 8. Principal cytokine mediator Measured in serum and urine Discriminate severe from mild cases on day 1

101. GENERAL COMPLICATIONS RESPIRATORY INSUFFICIENCY ADRS RENAL FAILURE DEPRESSED MYOCARDIAL FUNCTION ( MULTIPLE ORGAN FAILURE )

102. MECHANISMS OF GENERAL COMPLICATION PANCREATIC INFECTION COLON …..??? RLEASE OF ACTIVE INFLAMATORY MEDIATORS

103. INDICATION OF LAPAROTOMY…??

104. ACCEPTED INDICATIONS DIAGNOSIS IN DOUBT PERSISTENT BILIARY PANCREATITIS INFECTIVE PANCREATIC NECROSIS PANCREATIC ABSCESS

105. CONTROVERSIAL INDICATIONS > 50% STERILE PANCREATIC NECROSIS STABLE BUT PERSISTENT DISEASE DETERIORATION IN CLINICAL COURSE ORGAN SYSTEMIC FAILURE

106. WHAT IS THE OPERATION..?

107. UNDER SURGICAL OR MEDICAL !!??

108. !!! ! ! ! ! ?

109. Yours .... you..! YOU ..!! Me ..?? Your Case ... !!

110. RESPOSIBILITY RESPONSIBILITY ... !! RESPOSIBILITY D RESPONSIBILITY RESPONSIBILITY ... !! RESPONSIBILITY ... !! RESPONSIBILITY ... !!

111. PROGNOSIS RANSON,S CRITERIA APACHE II SCORING SYSTEM GLASCO CRITERIA < 3 RANSONS ,S CR. MORTALITY RATE 0.9 % . 3-4 ….19 % …..5-6 50% ….. > 6 ….90 %

112. It Is Nice To Be Important ..... But It Is More Important To Be Nice Mahatma ... Said Fazli Amin

113. THANK YOU !!!