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DR Fiaz Maqbool Fazili Lecturer, SIMS What Surgeons Should Know About Pancreatitis.

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Presentation on theme: "DR Fiaz Maqbool Fazili Lecturer, SIMS What Surgeons Should Know About Pancreatitis."— Presentation transcript:

1 DR Fiaz Maqbool Fazili Lecturer, SIMS What Surgeons Should Know About Pancreatitis

2 MAGNITUDE OF THE PROBLEM The disease may be mild and self limiting, 70-80% take course of edematous interstitial inflammation Necrotizing pancreatitis develops in % pts % will develop local or systemic complications Approx 1 in 4 pts who develop complications will die

3 WHAT IS THE BASIS OF PROBLEMS(PATHOLOGY) oNP shows interstitial edematous inflammation with EXTENSIVE NECROSIS OF PANCREATIC EXOCRINE AND ENDOCRINE PARENCHYMA,fatty necrosis of peripancreatic and retroperitoneal tissue compartment

4 PATHOLOGY (CONTD) Peripancreatic fluid collection of phospholipase,endtotoxin,prostacyclin, activated trypsin (TAP\),complement, thromboxane,elastase,TNFR and IL-6,8 Others(vasoactive and toxic substances

5 * AP & QUESTIONS WHAT IS THE CORRCT DIAGNOSIS? What is the prognosis? Are complications developing? Can an associated condition to be identified? What is the ideal timing for surgery?

6 OBJECTIVE To give pts of AP best chance of survival, from the outset to be managed by surgeon Identification of pts likely to develop complications Management (prevention)of systemic complications Timing and choice for surgical Intervention for gall stones or local complications

7 PANCREATITIS (terminology) MILD-uncomplicated recovery SEVERE-AP with evidence of failure of one or more systems, or local complication. These terms are defined retrospectively,when outcome is known Prospectively defined on the basis of scoring systems.Predicted Mild or Predicted Severe

8 ACUTE PANCREATITS-various terms COMPLICATED- local or systemic complications EDEMATOUS-Swollen, red,with or without fat necrosis;Histology fluid,debris,leukocytes present PERIPANCREATIC NECROSIS- Necrosis of retroperitoneal fat, other organs rarely involved, occasionally infarction by vascular thrombosis.This change may be present alone or may coexist with or be absent in presence of pancreatic necrosis

9 ACUTE NECROTIZING PANCREATITITS Definition Diagnosis CRITERIA Conservative approach or Surgical Intervention

10 AP-local complications …… contd Pancreatic necrosis; Patchy or diffuse superficial or parenchymal necrosis, unequivocally demonstrated by inspection after opening of the pancreatic capsule, or histological criteria; local or diffuse areas of non enhancement on CT, sterile necrosis Infected pancreatic necrosis ; Necrosis with positive bacterial cultures Pancreatic abscess; Loculated walled off collections of pus as a late complication of AP, usually after 3 weeks


12 A p MANIFESTATIONS(C0NT Extension into ; Retoperitoneum,perirenal spaces, mesocolon, major and minor omentum, mediastinum.

13 Bacterial contamination Risk of bacterial infection on necrotic tissue 60% in proven cases of NP Risk in ist week =25% Risk in 2 nd week = 35-40% Risk in 3 rd week =60% Organisms are Gram negative E-coli,Proteus,Pseudomonas,staphylococci

14 SYSTEMIC COMPLICATIONS o Respiratory- Interstitial pulmonary edema;gas transfer impairment,Pt may need ventilation o Renal-o liguria-require aggressive circulatory support,#Dialysis Cardiovascular- Hypotension, edema,aggressive fluid therapy and Ionotropes Disturbance in Haemopoiesis, Coagulation system, Endocrine systems

15 PANCREATITIS How to diagnose it? How to evaluate severity? RANSON CRITERIA IMRIES CRITERIA APACHE scoring GLASGOW Criteria Atlanta score Lab and Radiology Help ;

16 Diagnosis of Pancreatitis Clinical Diagnosis Lab studies; Serum amylase ;Levels Rise within 2-12hrs, o 3x times normal is cut off. (n IU/liter o levels normal in 2-3days. o Persistence of ^ levels >10days denote complication like cyst,abscess. o 5%cases no increase value

17 Diagnosis of pancreatitis(contd) Serum lipase ^^ 2x times the normal( IU/L) n=3-5days CR protein,LDH,Serum Neutrophil – elastase,IL-6, and alpha macroglobulin Trypsin like Immunoreactivity

18 RANSON CRITERIA Initial 24 hrs 1.Age >55 years 2.Glucose >than 200 mgm/dl 3.WBC > 16,000 cells/mic L 4.LDH >350 IU/liter 5.AST >250IU/liter Subsequent 48 hrs 1.Art o 2 tension <60mmHg 2.Bun Increase >8mg/dl 3.Ca < 8mg/dl 4.Base deficit >4meq/liter 5.Estimated fluid sequestration >6liters 6.Fall n Hct >10%

19 Mortality prediction (as per Ranson criteria) A. < 3 signs = 1% B. Three to Four signs=11% C. Five to six signs=33% D. >Six signs= 100%

20 IMRIE,S CRITERIA During first 24 hours 1.Age>55 yrs 2.WBC >15x 10 9 /l 3.Blood glucose >10mmol/l 4.Plasma Urea>16mmol/l 5.Pao 2 <8Kpa 6.Pl ca<2.0mmo/l 7.Pl albumin<32g/l 8.LDH>600 u/l(n=250) 9.AST or ALT >100 u/l

21 Apache II score(Sum of A+B+C) A=+4 to 0 points TEMP>41=4,<29=4 Mean Art Pr>160=4 <49=4 Heart & Resp rate OXYGENATION ART PH Ser Na,K,Creat, HCT,WBC GLASGOW COMA Score B=Age <44=0 pts >75=6points C=Chronic Health points H/o organ insufficiency Liver,CVS,Resp,Renal,,Immunocompromised APACHE SCORE42=90% Mort

22 APACHEII-variables 1. Temp 2. Mean Art Pressure 3. Heart Rate 4. Resp rate 5. Oxygenation(Pao 2) 6. Arterial Ph 1. Serum sodium 2. SerumPottasium 3. Serum creatinine 4. Haematocrit 5. WCC 6. Glasgow coma scale

23 GLASGOW CRITERIA Any time during First 48hrs after admission 1.WBC >15000 Cu/mm 2.Blood glucose>10mmol/l 3.BUN >16mmol/L 4.Art po 2,< 60mmHg 5.Ser ca. <2.0 ml/l 6.Ser Albumin<32gm/l 7.Ser LDH >600u/L(n=250) 8.AST Or ALT >200u/l

24 GLASGOW CRITERIA Any time during First 48hrs after admission; WBC >15000 Cu/mm Blood glucose>10mmol/l BUN >16mmol/L Art po 2,< 60mmHg Ser ca. <2.0 ml/l Ser Albumin<32gm/l Ser LDH >600u/L(n=250) AST Or ALT >200u/l

25 Comparison of scores Predicti on of complic ApacheRansonGlasgow Few hours More accurate Less 48hrs88%69%84% 72 hrs+++++ Dying ptRisingFalling

26 INTERSTITIAL AND NECROTIZING PANCREATITIS (Discrimination) Markers of Necroses C-reactive protein>120 mgm/L PMN-Elastase>120mgm/L PLA>15U/L PLA 2 >3.5U/L Dynamic angio – CT Guided needle aspiration of necroses for detection of bacteria

27 IDEAL PREDICTOR??? Accurate Simple Safe(non invasive) Rapidly formed Early in attack Reproducible Cheap Not influenced by etiology and co – morbidities Capable of monitoring course of disease and response to therapy

28 RADIOLOGY Plain Films Ultrasonography Sens;62-95%,Specif>95%, pancreas not visualized in> 40%pts CT scan;Sens 90% Specif+100% ERCP PTC. Pancreatitis is due to gallstone? Or Alcoholic?

29 CT severity index Ct gradePointsNecrosisPointsCtsi score* A0 B1NONE01 C2<30%24 D330-50%47 E4>50%610

30 The CT severity index-Balthazar et al FLUID COLLECTIONS-points 0-Normal pancreas 1-Gland enlargement 2-peripancreatic inflammation 3-one fluid collection 4-Multiple fluid collections Necrosis points 30% ---2pnts 30-50%--4pnts >50%----6pnt Total=10 points Predicted mortality Ctsi<3 3% Ctsi>7 17%

31 CTSI SCORE=CT GRADE+NECROSIS SCORE Acute pancreatitis CT grade ANormal pancreas BPancreatic enlargement CInflammation of peripancreatic fat DSingle peripancreatic fluid collection E two or more fluid collections or retroperitoneal air

32 CT findings in Acute Pancreatitis Enlargement of Gland Ill defined margins Abnormal enhancement Thickening of peripancreatic planes Blurring of fat planes Intra & retroperitoneal fluid collection Pleural effusion Pancreatic gas indicative of necrosis /abscess Pseudocyst formation

33 Indications of ERCP; In AP Preop evaluation with suspected traumatic pancreatitis to see Pancreatic duct disruption Pts with suspected biliary Pancreatitis and severe disease and not clinically improving by 24hrs after admission. Do ERCP for stone extraction

34 ERCP-indications (contd In pts >40 with no identifiable disease to rule out occult CBD stones,pancreatic or ampullary Ca or other causes of obstruction; Pts <40 at a post Cholecystectomy status or more than one attacks of unexplained pancreatitis

35 SYSTEMIC TREATMENTS Basic principles-ICU,Rest GIT and Pancreas,analgesia,oxygenation Pancreatic inhibition(Glucagon,Somatostatin) Antiproteases Antibiotics(cefuroxime) LEXIPAFANT Lavage Nutrition (Enteral route is safe& preferred ) Thoracic duct drainage

36 LEXIPAFANT-PAF antagonist Cause of organ failure and tissue damage in AP is activation of immune system involving interactions of cytokines and mediators.Role of PAF platelet activating factor is evident in pancreatic injury and SIRS LAXIPAFANT is PAF antagonist; Results are encouraging ;They reduce severity of organ failure. If given within 72 hrs

37 Operative Measures For AP A.Diagnostic laparotomy B.To limit the severity of pancreatic inflammation Biliary operations C.To interrupt the pathogenesis of complications Pancreatic drainage Pancreatic resection Peritoneal drainage

38 Operative measures(contg) D.To support the patient and treat complications Drainage of pancreatic abscesses Feeding jejunostomy To prevent recurrent pancreatitis

39 Indications Of Surgical intervention Diagnostic uncertainty Gall stone induced pancreatitis Pancreatic drainage and defunctioning Pancreatic resection Peritoneal Lavage Operation for complications


41 Bile duct stones-strategy Acosta (1974), recovered gall stones from Faeces of pts with gall stone pancreatitis. Neptolemos (1989) ;Passage of stone through ampulla precipitates pancreatitis attack, persistence of stones in CBD; Pt is at risk of complications and death Early surgery or to deal with CBD stones endoscopically(ERCP)14 %pts of AP have coexisting cholangitis

42 Early or Delayed OPERATION Pts who have early Cholecystectomy (48hrs) of admission with AP as compared to pts who were treated conservatively, D/C and readmission. Mort was 2% in early surgery group and 16 % in retrospective group, (same adm OR) Ideal timing ;Those who Advocate early OR, say that it removes potential septic focus in GB,remove CBD stones causing CBD obst and pptng pancreatitis,Thus shortens hospital stay

43 EARLY OR DELAYED SURGERY Early operation ;good results mortality only2%(same admission Cholecystectomy) Delayed surgery mort 16% Ideal timing?still debatable

44 DELAYED OPERATION Delay operation(until 7 to 10days) till acute attack subsides Most of CBD stones will pass spontaneously and don t need OR Most pts have mild pancreatitis and don t need early OR,( indeed there won be evidence of inflammation till one week ) Complications of early operation are high

45 Timing OF Operation IN Gall Stone Pancreatitis Mild pancreatitis: Operated At Any Stage during first admission Severe disease.Cholecystectomy during first admission, timing depends on clinical indicators

46 Timing of Surgery-contd RECOVERING PT.Allow pt to settle completely before elective early operation is taken prior to discharge. UNSTABLE PT- Who will require surgery to deal with local complications of pancreas, Cholecystectomy to be performed at this time Early Cholecystectomy within hours of admission is best avoided in these all patients

47 NON respondents of medical treatment Persistent or increase signs of pulmonary, Renal or cardio vascular insufficiency, Develops sepsis syndrome during max of 3 days of ICU, PT belongs to non responders with high risk of morbidity and mortality. Switch from Medical to surgical treatment.

48 Indications of Operation IN NP Clinical criteria Surgical acute abdomen Sepsis syndrome Shock syndrome Non response to ICU Morphologic +Bacteriologic Infected necroses Extended pancreatic necrosis>50% Extnd. intrapancreatic +retroperitoneal necroses Stenosis of CBD,Duodenum, large bowel

49 Technique of Debridement Closed cavity Lavage Open abdomen Surgical drainage Posterior approach Pancreatic resection

50 Surgical Approaches-choices Limited Peritoneal exploration, digital debridement, closed cavity drainage (Beger et al) Combination of ext debridement with closed cavity drainage Bradley approach Thorough and extensive surgical debridement of retro perit space, packing of abdomen, which is left open, subsequent changes of packs is a planned procedure.

51 Necrosectomy +CLOSED CAVITY LAVAGE Surgical debridement – Necrosectomy – supplemented by intraoperative and post operative closed continuous local Lavage of of the lesser sac and the necrotic cavities.(mort8 – 15%) Debridement- either digital or by the careful use of of instruments – Elimination of all demarcated,devitalized tissue, preserving the vital pancreatic parenchyma.

52 Necrosectomy+CC Lavage(contd) Thorough haemostasis with monofilament transfixing stitches. Don t remove every gram of devitalized tissue Extensive intraoperative Lavage is performed with 6-12 L of normal saline Post operative closed continuous local Lavage with two large double lumen silicone rubber tubes (34) are inserted in R and L retro peritoneum

53 Necr+Closed Lavage Drains are at level of RP space in L and R retroperitoneum. Gastro colic and duodenocolic ligaments are sutured to create closed system. Drains in pelvis or gutters Monitor Lavage fluid for enzymes,toxins,etc When to Stop Lavage -no signs of AP,culture negative., fluid less enzymes or necr tissue output is <7gm /24 hrs

54 OPEN ABDOMEN approach o Debridement and open packing. o Disadvantages;Prolonged ICU multiple dressings,Multiple reoperations o Int. fistulas 30 %, gastric outlet obst, ileus, Stenosis of T colon, incisional hernia(29%) o Pancr. fistula % o Mort is 28%

55 SURGICAL DRAINAGE Extensive debridement to remove necrotic tissue followed by Abd. closure with drains Disadvantages=High reoperation rate Suitable for pts in whom no further intervention is required. No benefit over c c drainage Mort is <25%

56 POSTERIOR APPROACH Pancreatic necrosis through L retro perit approach No advantage in terms of complications, restriction in incision,cant drain Abdominal ascites

57 Pancreatic resection Hardly ever warranted except as a part of Necrosectomy No beneficial effect in terms of systemic complications. Incidence of DM 100%, high incidence of neuropathy (Eriksson 1992)

58 Pancreatic abscess Late stage Wide surgical exploration +closed drainage or open packing Hemorrhage and fistula are common complications

59 Role of Antibiotics in AP Traditional teaching is Prophylactic antibiotics do not prevent abscess- Mezlocillin, Metrionidazole, Imipnem good concentration in pancreatic juice Cefotaxime, Ceftazidime Clindamycin, Ciprofloacin good levels in p. juice They can limit rate of infection of this necr material(Bossi1992)

60 Pseudo cyst Delineation of main Pancreatic duct by ERP if no communication -drain by ERP If main duct is abnormal Stricture Or Truncated – Surg. Drainage Rarely normal P.Duct communicating with Pseudo Cyst – Drain Percut CT control (Recurrence =50%)

61 Conclusion Management of AP is complex Mortality is high-Realization Increasing Dx procedures available has not simplified decisions about timing of operation or choice of technique. Individualized approach IS NECESSARY Decision based on clinical judgment rather than on numerical or imaging. SURGEON IS THE BEST TO MANAGE as he has CLINICAL AND SURGICAL EXPERTISE

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