DR Fiaz Maqbool Fazili Lecturer, SIMS

What Surgeons Should What Surgeons Should Know About Know About PancreatitisPancreatitis

MAGNITUDE OF THE PROBLEM

The disease may be mild and self limiting, 70-80% 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

WHAT IS THE BASIS OF PROBLEMS(PATHOLOGY)

o NP shows interstitial edematous inflammation with EXTENSIVE NECROSIS OF PANCREATIC EXOCRINE AND ENDOCRINE PARENCHYMA,fatty necrosis of peripancreatic and retroperitoneal tissue compartment

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

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?

OBJECTIVETo give pts of AP best chance of survival, from the outset to be managed by surgeon

Identification of pts likely to develop complicationsManagement (prevention)of systemic complicationsTiming and choice for surgical Intervention for gall stones or local complications

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

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

ACUTE NECROTIZING PANCREATITITS Definition Diagnosis CRITERIA Conservative approach or Surgical

Intervention

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

MANIFESTATIONS OF AP LOCAL;LOCAL;

MILD; EDEMA, INFLAMMATION, NECROSIS

SEVERE; PHLEGMON, NECROSIS, HYG, INFECTION,

FLUID COLLECTION, ABSCESS

A p MANIFESTATIONS(C0NT• Extension into ;

• Retoperitoneum,perirenal spaces, mesocolon, major and minor omentum, mediastinum.

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

SYSTEMIC COMPLICATIONSo Respiratory-Interstitial pulmonary

edema;gas transfer impairment,Pt may need ventilation

o Renal-oliguria-require aggressive circulatory support,#Dialysis

Cardiovascular-Hypotension, edema,aggressive fluid therapy and Ionotropes

Disturbance in Haemopoiesis, Coagulation system, Endocrine systems

PANCREATITIS How to diagnose it?

How to evaluate severity?RANSON CRITERIAIMRIES CRITERIAAPACHE scoringGLASGOW CriteriaAtlanta scoreLab and Radiology Help ;

Diagnosis of PancreatitisClinical Diagnosis Lab studies;

Serum amylase;Levels Rise within 2-12hrs,

o 3x times normal is cut off . (n35-118 IU/liter

o levels normal in 2-3days. o Persistence of ^ levels >10days denote complication like cyst,abscess.

o 5%cases no increase value

Diagnosis of pancreatitis(contd)

Serum lipase ^^ 2x times the normal( 2.3-20.0 IU/L) n=3-5days

CR protein,LDH ,Serum Neutrophil –elastase,IL-6, and alpha macroglobulin

Trypsin like Immunoreactivity

RANSON CRITERIA Initial 24 hrs

1.Age >55 years2.Glucose >than 200 mgm/dl3.WBC > 16,000 cells/mic L4.LDH >350 IU/liter5.AST >250IU/liter

Subsequent 48 hrs1.Art o2tension <60mmHg2.Bun Increase >8mg/dl3.Ca < 8mg/dl4.Base deficit >4meq/liter5.Estimated fluid sequestration >6liters6.Fall n Hct >10%

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%

IMRIE,S CRITERIA During first 24

hours1.Age>55 yrs2.WBC >15x 10 9/l3.Blood glucose >10mmol/l4.Plasma Urea>16mmol/l5.Pao2<8Kpa

6.Pl ca<2.0mmo/l7.Pl albumin<32g/l8.LDH>600 u/l(n=250)9.AST or ALT >100 u/l

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

OXYGENATIONART PHSer 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

APACHEII-variables

1. Temp2. Mean Art

Pressure3. Heart Rate4. Resp rate5. Oxygenation(Pao

2)

6. Arterial Ph

1. Serum sodium2. SerumPottasium3. Serum creatinine4. Haematocrit5. WCC6. Glasgow coma

scale

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

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

Comparison of scores

Prediction of complic

Apache Ranson Glasgow

Few hours

More accurate

Less Less

48hrs 88% 69% 84%

72 hrs +++ ++ ++

Dying pt

Rising Falling Falling

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

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

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?

CT severity index

Ct grade

Points Necrosis

Points Ctsi score*

A 0

B 1 NONE 0 1

C 2 <30% 2 4

D 3 30-50% 4 7

E 4 >50% 6 10

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%

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

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

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

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

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

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

Operative Measures For APA.Diagnostic laparotomyB.To limit the severity of pancreatic inflammation

Biliary operations

C.To interrupt the pathogenesis of complications

Pancreatic drainagePancreatic resectionPeritoneal drainage

Operative measures(contg)

D.To support the patient and treat complications

Drainage of pancreatic abscessesFeeding jejunostomy

To prevent recurrent pancreatitis

Indications Of Surgical intervention Diagnostic

uncertainty Gall stone induced

pancreatitis Pancreatic drainage

and defunctioning Pancreatic

resection Peritoneal Lavage

Operation for complications

GALL STONE PANCREATITIS

TIMING OF SURGERY TRADITIONAL APPROACH

EARLY OR DELAYED

TWO DAYS OR TWO WEEKS

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

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

EARLY OR DELAYED SURGERY Early operation ;good results

mortality only2%(same admission Cholecystectomy)

Delayed surgery mort 16%

Ideal timing?still debatable

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

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

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 48-72 hours of admission is best avoided in these all patients

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.

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

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

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.

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.

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

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

OPEN ABDOMEN approacho 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%

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%

POSTERIOR APPROACH Pancreatic necrosis through L

retro perit approach

No advantage in terms of complications, restriction in incision,cant drain Abdominal ascites

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)

Pancreatic abscess Late stage Wide surgical exploration +closed

drainage or open packing Hemorrhage and fistula are

common complications

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)

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%)

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