DR Fiaz Maqbool Fazili Lecturer, SIMS What Surgeons Should Know About Pancreatitis.
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Transcript of DR Fiaz Maqbool Fazili Lecturer, SIMS What Surgeons Should Know About Pancreatitis.
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DR Fiaz Maqbool Fazili Lecturer, SIMS
What Surgeons Should What Surgeons Should Know About Know About PancreatitisPancreatitis
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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
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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
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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
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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?
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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
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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
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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
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ACUTE NECROTIZING PANCREATITITS Definition Diagnosis CRITERIA Conservative approach or Surgical
Intervention
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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
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MANIFESTATIONS OF AP LOCAL;LOCAL;
MILD; EDEMA, INFLAMMATION, NECROSIS
SEVERE; PHLEGMON, NECROSIS, HYG, INFECTION,
FLUID COLLECTION, ABSCESS
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A p MANIFESTATIONS(C0NT• Extension into ;
• Retoperitoneum,perirenal spaces, mesocolon, major and minor omentum, mediastinum.
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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
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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
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PANCREATITIS How to diagnose it?
How to evaluate severity?RANSON CRITERIAIMRIES CRITERIAAPACHE scoringGLASGOW CriteriaAtlanta scoreLab and Radiology Help ;
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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
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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
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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%
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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%
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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
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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
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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
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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
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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
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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
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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
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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
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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?
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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
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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%
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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
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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
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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
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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
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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
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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
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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
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Operative measures(contg)
D.To support the patient and treat complications
Drainage of pancreatic abscessesFeeding jejunostomy
To prevent recurrent pancreatitis
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Indications Of Surgical intervention Diagnostic
uncertainty Gall stone induced
pancreatitis Pancreatic drainage
and defunctioning Pancreatic
resection Peritoneal Lavage
Operation for complications
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GALL STONE PANCREATITIS
TIMING OF SURGERY TRADITIONAL APPROACH
EARLY OR DELAYED
TWO DAYS OR TWO WEEKS
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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
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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
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EARLY OR DELAYED SURGERY Early operation ;good results
mortality only2%(same admission Cholecystectomy)
Delayed surgery mort 16%
Ideal timing?still debatable
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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
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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
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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
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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.
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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
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Technique of Debridement Closed cavity Lavage Open abdomen Surgical drainage Posterior approach Pancreatic resection
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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.
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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.
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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
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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
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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%
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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%
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POSTERIOR APPROACH Pancreatic necrosis through L
retro perit approach
No advantage in terms of complications, restriction in incision,cant drain Abdominal ascites
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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)
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Pancreatic abscess Late stage Wide surgical exploration +closed
drainage or open packing Hemorrhage and fistula are
common complications
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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)
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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%)
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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