Transcript Acute Necrotizing Pancreatitis

What Surgeons Should
Know About Pancreatitis
DR Fiaz Maqbool Fazili
Lecturer, SIMS
MAGNITUDE OF THE
PROBLEM
 The disease may be mild and self
limiting,
70-80% take course of
edematous interstitial inflammation
 Necrotizing pancreatitis develops in 2025% 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


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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?
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
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

Pancreatic abscess;Loculated walled off
positive bacterial cultures
collections of pus as a late complication of AP, usually
after 3 weeks
MANIFESTATIONS OF AP

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%
nd week = 35-40%
 Risk in 2
rd week =60%
 Risk in 3
Organisms are Gram negative
E-coli,Proteus,Pseudomonas,staphylococci
SYSTEMIC COMPLICATIONS
o
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 CRITERIA
IMRIES CRITERIA
APACHE scoring
GLASGOW Criteria
Atlanta score
Lab and Radiology Help ;
Diagnosis of Pancreatitis
Clinical 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 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%
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 hours
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
Apache II score(Sum of
A+B+C)

A=+4 to 0 points
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
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


C=Chronic Health
points


>75=6points
H/o organ insufficiency
Liver,CVS,Resp,Renal,
,Immunocompromised
APACHE SCORE42=90%
Mort
APACHEII-variables
1.
2.
3.
4.
5.
6.
Temp
Mean Art Pressure
Heart Rate
Resp rate
Oxygenation(Pao2)
Arterial Ph
1.
2.
3.
4.
5.
6.
Serum sodium
SerumPottasium
Serum creatinine
Haematocrit
WCC
Glasgow coma
scale
GLASGOW CRITERIA

Any time during First 48hrs after
admission

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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;

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

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
Predicti Apache
on of
complic
Ranson
Glasgow
Few
hours
48hrs
More
Less
accurate
88%
69%
Less
72 hrs
+++
++
++
Falling
Falling
Dying pt Rising
84%
INTERSTITIAL AND NECROTIZING
PANCREATITIS (Discrimination)

Markers of Necroses



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

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???
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Accurate
Simple
Safe(non invasive)
Rapidly formed
Early in attack
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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%
10
6
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
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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

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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
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

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

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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 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
Operative measures(contg)
D.To support the patient and treat
complications
Drainage of pancreatic abscesses
Feeding 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

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
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 approach
o
o
o
o
o
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%
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 abscessMezlocillin, 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



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

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