Acute pancreatitis Szentkereszty Zs. MD. Ph. D. Med. habil. UD MHSC Inst. Surgery.
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Transcript of Acute pancreatitis Szentkereszty Zs. MD. Ph. D. Med. habil. UD MHSC Inst. Surgery.
![Page 1: Acute pancreatitis Szentkereszty Zs. MD. Ph. D. Med. habil. UD MHSC Inst. Surgery.](https://reader035.fdocuments.in/reader035/viewer/2022062308/56649d765503460f94a57644/html5/thumbnails/1.jpg)
Acute pancreatitis
Szentkereszty Zs.
MD. Ph. D. Med. habil.
UD MHSC Inst. Surgery
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Atlanta classification I.
Mild acute pancreatitis(< Ranson 3, < APACHE-II 8, no local
and/or systemic complication)
Severe acute pancreatitis(> Ranson 3, > APACHE-II 8, local and/or
systemic complication)
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Atlanta classification V. local complications
Pancreas abscess
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Atlanta classification VI. local complications
Acute pseudocyst
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Atlanta classification VI. systemic complications
• SIRS/MODS/MOF
• ARDS
• Renal failure
• DIC
• sepsis
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Modified Atlantai classification
First phase (1th. week)
• SIRS
• MODS/MOF– Mortality spice
• Inflammation, ischemy
– Oedema
– Necrosis
– Liquification
– Fluid collections
Second phase (2th. week)
• Recovery or no
• Mortality spice (infection)
• Local complications
• Local infection’s systemic manifestation (sepsis)
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Modified Atlantai classification
First phase (1th. week)
• Characterizated by systemic complications (MODS/MOF)
• Clinical classification
Second phase (2th. week)
• Characterizated by
local complications
• Morphologic classification
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Modified Atlantai classification
Criterions of acute pancreatitis
1. Severe acute pain
2. Elevated serum Amylase and/or Lipase levels for minimun three times
3. Typical lesions on CE-CT scan
Minimum 2 criterions needed
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Modified Atlantai classification
Scoring
• Puls number > 90/min
• Central temperature > 38 ºC < 36 ºC
• WBC < 4 or > 12 G/L
• Breathong rate > 20/min
• pCO2 < 32 Hgmm
• SIRS
• APACHE-II, Ranson, CRP, etc.
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Modified Atlantai classification
Local complications
1. Interstitial oedematous pancreatitis (IEP)• Oedema
• Normal contrast enhance
• Acute peripancreatic fluid collection (endoscopic US, MRI for verify or exclude the necrosis)
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Modified Atlantai classification
Local complications
2. Pancreatic necrosis• Localization (pancreatic and/or peripancreatic)
• Sterile or infected
• Staging (Balthazar score: < 30%; 30-50%; > 50%)
• Retrocolic fluid, thickening of the mesenterium
• Necrosis-liquified necrosis (post-necrotic pancreatic fluid collection PNPFC)
• Infection (gas bubbles, FNA)
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Sterile necrosis
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Infected necrosis
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Modified Atlantai classification
Local complications
3. Acute peripancreatic fluid collections (APFC)• No solide content, concomitant of IEP
• No true wall
• Sterile or infected
• Generally sterile
• Spontaneous resolving tendency
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Acute peripancreatic fluid collection
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Modified Atlantai classification
Local complications
4. Post-necroticus pancreatic/peripancreatic fluid collection (PNPFC)• Solid content in the fluid, concomitant of PN
• Develeopes after 3-6 weeks
• Walled-off pancreatic necrosis (WOPN)
• Sterile or infected- gas bubble, FNA
• Generally sterile
• Spontaneous resolving tendency
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Modified Atlantai classification
Local complications
5. Pancreatic pseudocyst• Developes after 4-6 weeks• Developement from APFC• No solide contant• Well definied wall
• Sterile or infected- gas bubble, FNA
• Generally sterile• No spontaneous resolving tendency
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Etiology
• Alcohol
• Gallstone disease
• Hyperlipidaemy
• Hypercalcaemy
• Trauma
• Viral infectuions
• Idiopathic
• Ductal obstruction
– Tumour, diseases of the papilla
• Postoperative
• Iatrogenic
– ERCP
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Sex & age ratio
0
5
10
15
20
25
No. Of patients
0-20 21-30 31-40 41-50 51-60 61-
years
male
female
all
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Complaints
• Pain
• Nausea, vomiting
• Tachycardia
• fever
• Swelling
• Paralytic ileus
• Hypotension, shock
• Renal failure
• Dyspnoe
• Coagulopathy (DIC)
• Cullen sign
• Grey-Turner sign
• Jaundice
• Sepsis
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Diagnosis I.
• Case history
• Complaints
• Laboratory– Elevated serum and urine Amylase, serum Lipase
levels
– Trypszin, Trypszinogén α-2, TAP, Foszfolipase,
– WBC, CRP, Htc, Liver function, serum Ca+, ASTRUP levels
– TNFα, IL-6, PCT, Coagulation, stb.
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Diagnosis II.
• Native chest and abdominal X-ray
• US
• CE-CT
• MR
• Leukocyta scintigraphy (if needed)
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Diagnosis III.
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Diagnosis IV.
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Diagnosis V.
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Diagnosis VI.
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Mild acute pancreatitis
Non bacterial origin
Pathologic laesion (oedema)
Local „disease”
Recovery for conservative treatment (generally)
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Mild acute pancreatitis
Conservative treatment
• „put the pancreas in rest”
• Gastric tube (suction)
• Ice/cold locally
Conservative treatment
• Intravenous fluids
• PPI
• Pain killers
• spamolithics
• EST
• Cholecystectomy
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Severe acute pancreatitis
Non bacterial origin
Pathologic laesion (eg. necrosis)
In origin local than general disease
(SIRS, MODS/MOF )
Septic complications
(abscess)
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Severe acute pancreatitis
Patomechanism
• Autodigestive theory– A Trypsonogen-trypsin system activation in the
gland parenchyma– membrane damage of the ductal cells – Damage of the defensive system
• Ductal pressure elevation (in biliary panreatitisben)• The alcohol decreases the sensitivness of the acinal cells for
cholecystokinin, membrane damage of zymogen granulums
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A severe acute (necrotisans) pancreatitis
Patomechanism
• Autodigestive theory– Autodigestion, release of free oxygen radics– Tissue damage– Migration of monocytes, macrophags and neutrophyl
granulocyts- cytokine secretion• TNF, IL-1, IL-6, IL-8, INF-ok, PAF, Colonia stimulants, CICAM-1,
– Mediators– Vasoactive agents
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A severe acute (necrotisans) pancreatitis
Patomechanism
• Autodigestion– Local effects
• + NO and PAF increase the permeability of the small vessels, causes edema and decreases the microcirculation of the pancreas
• Systemic effects
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A severe acute (necrotisans) pancreatitis
Patomechanism
• Microcirculation theory– Local effect
• + NO and PAF increase the permeability of the small vessels, causes edema and decreases the microcirculation of the pancreas
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A severe acute (necrotisans) pancreatitis
Patomechanism
• Systemic effects– The vasoactive agents and cytikines causes organ failure (SIRS)
– MODS than MOF• Shock
• Renal failure
• DIC
• ARDS – alveolar microthrombuses
– Lecitinase causes the destruction of surfactan
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Treatment I.
Konservative treatmentKonservative treatment
• ICU• Fluid and electrolyte resuscitation• Put the pancreas in rest• Painkillers, spasmolytics, EDA• Treatment of SIRS/MODS/MOF
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Konservative treatment
• Fluid and elextrolyte resustitation (4-6000 ml/day)
• Blood gas correction
• Pain killers
• EDA
• Naso-gastric tube
• H2 blocker, PPI
k o n zerv a tív k ezelé s
en y h e
m û té t
szö v õ d m én y(v érzés , p erf o ra tio )
k o n zerv a tív k ezelé s
s teril n ecro s i s
m û té t
n em g y ó g y u l g y ó g y u l
P P D
sep ticu s n ecro s is
A n tib io tik u mN a so -jeu n á lis tá p lá lásP P D -fo ly a d ék g y ü lem
In ten zív o sztá l yC T (n ecro s is )
sú ly o s
A P A C H E -I IR a n so n sco r e
D g .: a cu t p a n crea titi sk lin ik um
la b o rU H
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Conservative treatment
• Antibiotic prophylaxisAntibiotic prophylaxis imipenem/cilastatin 3x500 mg
• AB therapy
• Thoracocentesis
• Chest tube drainage
• Treatment of MODS Thrombosis prophylaxis
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Treatment
Early enteral jejunal tube feedingEarly enteral jejunal tube feeding
• Scientific basis– Bowel mucosa atrophia– Bacterium translocation– CCK-PZ system– Disadventages of TPN
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Naso-jejunal tube feedeing
• Within 48 hour insert the naso-jejunal feeding tube
• Next day start the feeding
• Increase the dosage of nutrients
k o n zerv a tív k ezelé s
en y h e
m û té t
szö v õ d m én y(v érzés , p erf o ra tio )
k o n zerv a tív k ezelé s
s teril n ecro s i s
m û té t
n em g y ó g y u l g y ó g y u l
P P D
sep ticu s n ecro s is
A n tib io tik umN a so -jeu n á lis tá p lá lásP P D -fo ly a d ék g y ü lem
In ten zív o sztá l yC T (n ecro s is )
sú ly o s
A P A C H E -I IR a n so n sco r e
D g .: a cu t p a n crea titi sk lin ik um
la b o rU H
![Page 40: Acute pancreatitis Szentkereszty Zs. MD. Ph. D. Med. habil. UD MHSC Inst. Surgery.](https://reader035.fdocuments.in/reader035/viewer/2022062308/56649d765503460f94a57644/html5/thumbnails/40.jpg)
Naso-jejunal tube feedeing
• 25-30 kcal/kg/day (1500-2000 ml nutrien)
• Enteral pump
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Treatment
Antibioticum prophylaxisAntibioticum prophylaxis
• Scentific basis:– Adevantage only in severe cases– Spectrum of the bacterial agents in septic
complications– Effective antibiotics– inough penetration and tissue concentration– Imipenem, Fluorokinolons
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Treatment
Percutaneous peripancreatic drainagePercutaneous peripancreatic drainage
• Scientific basis:– Developement of interventional radiology– Good effects of other fluid drainages– Later the large fluid collection was an indication
for surgery
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Percutaneous peripancreatic drainage
Acute peripancreatic fluid collections
• PPD
35%
• In 20% more than one drain
k o n zerv a tív k ezelé s
en y h e
m û té t
szö v õ d m én y(v érzés , p erf o ra tio )
k o n zerv a tív k ezelé s
s teril n ecro s i s
m û té t
n em g y ó g y u l g y ó g y u l
P P D
sep ticu s n ecro s is
A n tib io tik umN a so -jeu n á lis tá p lá lásP P D -fo ly a d ék g y ü lem
In ten zív o sztá l yC T (n ecro s is )
sú ly o s
A P A C H E -I IR a n so n sco r e
D g .: a cu t p a n crea titi sk lin ik um
la b o rU H
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Percutaneous peripancreatic drainage
• Becterium stain and resistency
• Lavage of the drains
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Percutaneous peripancreatic drainage
• US observation
• Remove if the drained fluid is les than 20-30 ml/day and it is sterile
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Treatment
SurgerySurgery
• Scientific basis:– Early operation has a high rate of mortality,
reoperations and complications– Thre known of the spread of necrosis– The developement of pancreas surgery
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Surgery
Indication for surgeryIndication for surgery• Septic necrosis• Failure of PPD • Failure of conservative
treatment of MODS• Surgical complications
(perforation, bleeding, peritonitis)
• IAH/ACS
k o n zerv a tív k ezelé s
en y h e
m û té t
szö v õ d m én y(v érzés , p erf o ra tio )
k o n zerv a tív k ezelé s
s teril n ecro s i s
m û té t
n em g y ó g y u l g y ó g y u l
P P D
sep ticu s n ecro s is
A n tib io tik u mN a so -jeu n á lis tá p lá lásP P D -fo ly a d ék g y ü lem
In ten zív o sztá l yC T (n ecro s is )
sú ly o s
A P A C H E -I IR a n so n sco r e
D g .: a cu t p a n crea titi sk lin ik u m
la b o rU H
![Page 48: Acute pancreatitis Szentkereszty Zs. MD. Ph. D. Med. habil. UD MHSC Inst. Surgery.](https://reader035.fdocuments.in/reader035/viewer/2022062308/56649d765503460f94a57644/html5/thumbnails/48.jpg)
Surgary
Early operation 10-15%Acute abdomenLate operation 85-90%Septic necrosis 60%MOF 20%PPD failure PPD failure 30%30%
Daitgnosis of septic necrosisFNA, PPD , PCT
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Surgery
TecniqueTecnique
• Curved upper transversal laparotomy
• Blunt necrectomy• Exploration of retrocolic
spaces• Cholecystectomy + cystic
drain • Postoperative closed bursa
omentalis lavage
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Surgery
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Surgery
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Surgery
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Surgery
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Treatment
The treatment of biliary ANPThe treatment of biliary ANP
• Scientific basis:– The use of ERCP/EST routinly– The effect, timing and results of EST– The timing of cholecystectomy– The decompression of common bile duct
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The treatment of biliary pancreatitis
• EST is possible only in 70% of the cases
• Necrectomy, cholecystectomy and cystic duct drain
• Elective cholecystectomy
E lek tívC h o lecy s tecto m i a
k o n zerv a tív k ezelé s
en y h e
M û té tN ecre cto m i a
C h o lecy s tecto m i a
szö v õ d m én y(v érzés , p erf o ra tio )
E lek tívC h o lecy s tecto m i a
k o n zerv a tív k ezelé s
steril n ecro s i s
N ecre cto m i aC h o lecy s tecto m i a
n em g y ó g y u l
E lek tívC h o lecy s tecto m i a
g y ó g y u l
P P D
szep tik u s n ek ró zis
K o ra i E STA n tib io tik um
N a so -jeju n a lis tá p lá lá sP P D -fo ly a d ék g y ü lem
In ten zív o sztá l yC T (n ecro s is )
sú ly o s
A P A C H E -I IR a n so n sco r e
D g .: a cu t b ilia ris p a n crea titisk lin ik um
la b o rU H