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

2. MAGNITUDE OF THE PROBLEM
The disease may be mild and self limiting, % take course of edematous interstitial inflammation
Necrotizing pancreatitis develops in 20-25% pts .
20-30% will develop local or systemic complications
Approx 1 in 4 pts who develop complications will die

3. WHAT IS THE BASIS OF PROBLEMS(PATHOLOGY)
NP shows interstitial edematous inflammation with EXTENSIVE NECROSIS OF PANCREATIC EXOCRINE AND ENDOCRINE PARENCHYMA,fatty necrosis of peripancreatic and retroperitoneal tissue compartment
why everyboy is scared o f this dreadful disease. what hapens and what goes wrong in this organ panrceasand waht is the cause of this widespread organ involvement. there is vasoactive and toxic substanes release,INFLAMMTORY MEDIATORS

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
We shall talk about some trminolgu used during discuusing acute pancreatitis. As we talked pancreatitis

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

11. MANIFESTATIONS OF AP LOCAL; MILD; EDEMA, INFLAMMATION, NECROSIS
SEVERE;
PHLEGMON, NECROSIS, HYG, INFECTION, FLUID COLLECTION, ABSCESS

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 2nd week = 35-40%
Risk in 3rd week =60%
Organisms are Gram negative E-coli,Proteus,Pseudomonas,staphylococci

14. SYSTEMIC COMPLICATIONS
Respiratory-Interstitial pulmonary edema;gas transfer impairment,Pt may need ventilation
Renal-oliguria-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,
3x times normal is cut off . (n IU/liter
levels normal in 2-3days.
Persistence of ^ levels >10days denote complication like cyst,abscess.
5%cases no increase value
Pancreatitis is a clinical diagnosis , pain ra s 22 page 147done by exclusion, as many acute abdominal catstripohes mimic it.Serum amylase is a non specific marker getting increaed in many acute abdominal conditions, non abdominal conditions like peforated dU, Mes vas occlusion, Ectopic pregnacy, salvary tumours

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 o2tension <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 6.Pl ca<2.0mmo/l
1.Age>55 yrs
2.WBC >15x 10 9/l
3.Blood glucose >10mmol/l
4.Plasma Urea>16mmol/l
5.Pao2<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= <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 Temp Mean Art Pressure Heart Rate Resp rate
Oxygenation(Pao2)
Arterial Ph
Serum sodium
SerumPottasium
Serum creatinine
Haematocrit
WCC
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 po2,< 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 po2,< 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 Prediction of complic Apache Ranson Glasgow
Few hours
More accurate
Less
48hrs
88%
69%
84%
72 hrs
+++ ++
Dying pt
Rising
Falling

26. INTERSTITIAL AND NECROTIZING PANCREATITIS (Discrimination)
Markers of Necroses
C-reactive protein>120 mgm/L
PMN-Elastase>120mgm/L
PLA>15U/L
PLA2>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
When you have more than one method that means the ideal one is still in vogueMultiple factor scoring system categorises group of pts as predicted mild or severe .These categories sholud not be confused with actual outcome There is need for a predictive system that gives an individual risk of comlications the best accuracy that has been achieved is of orderof that is one fifth to one quarte are of ots prediction is incorrect

28. RADIOLOGY Plain Films Ultrasonography CT scan;Sens 90% Specif+100%
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 grade Points Necrosis Ctsi score* A B 1 NONE C 2B 1
NONE C 2
<30% 4 D 3
30-50% 7 E
>50% 6 10
Best known is apACHE !!, MULTIVAREIATE SCORING SYSTEM TAKES ACCOUNT PT AGE , ROUTINE BLOOD TESTS CAN BE PERFORMED ON ADMISSION AND SEQUENTIALLY PREDICTING ORGAN FAILURE AND PANCR NECROSES.SUP TO SAPS SIMPLOIFIES ACUTE PHYSIOLOGIC SCORE.READ RECENT ADVANCES21 PAGE126

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% pnts
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
A Normal pancreas
B Pancreatic enlargement
C Inflammation of peripancreatic fat
D Single 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
since we dont have a specific and effective medical phrmocotherapy for Ap mngmnt has bsed on generally accepted principles of ICUtreat, Phrmocolgic analgesia ,fluid and electrolyte .Sp attention to pulmon, renal, cardio circilatorynfunctions replacement.basic and initial treatment is consravitve AIP wil respond in 2 weeks. Analgesia., Antiprotease therapy no role as it is SIRS which is causing sytemic pronblems.Ineffective therpy aprotinin, gabexate also tried.Studies of glucagon, somatostatin,octeroide all have yielded negative findings.Antibiotics in severe disease.Rduction in comlication selective gut decontamination and cE.rest the pancreas to prevent wosening of damage appears false. Depriving te gut lumen of nutrients impars gut mucosal barrier function and exacerberate the problem of trans location.parnteral oute exacerbrates exacebates severe pancritis by direct stm o panc scr du to increased nutrent levels in blood

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

40. GALL STONE PANCREATITIS
TIMING OF SURGERY
TRADITIONAL APPROACH
EARLY OR DELAYED
TWO DAYS OR TWO WEEKS
Gall stones commonest cause. Timing of or, posbility of inluencing course by ear biliary interventionb.clearing duct surgically or by ercp.traditional aproach was conservative during attack, d/c from hospital readmit for elective or after recovery 6w to 6m. Jutification was to settle inflammation.

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
The protocol which I follow is

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.
Cl decision making in pts with complicated curse of NP includes ong local and long k=lasting systems organ complcations on pts response ti iCU with tegad to pulmon, renal. Cadio vascular dysfunctions,n improve

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
Broadly speaking h. brger3 approaches limied peritoneal explor, digitl debriement, closed cavity irrigation,bradley thor

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