acute pancreatitis szentkereszty zs. md. ph. d. med. habil. ud mhsc inst. surgery

Acute pancreatitis

Szentkereszty Zs.

MD. Ph. D. Med. habil.

UD MHSC Inst. Surgery

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)

Atlanta classification V. local complications

Pancreas abscess

Atlanta classification VI. local complications

Acute pseudocyst

Atlanta classification VI. systemic complications

• SIRS/MODS/MOF

• ARDS

• Renal failure

• DIC

• sepsis

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)


First phase (1th. week)

• Characterizated by systemic complications (MODS/MOF)

• Clinical classification

Second phase (2th. week)

• Characterizated by

local complications

• Morphologic 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


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.


Local complications

1. Interstitial oedematous pancreatitis (IEP)• Oedema

• Normal contrast enhance

• Acute peripancreatic fluid collection (endoscopic US, MRI for verify or exclude the necrosis)


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)

Sterile necrosis

Infected necrosis


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

Acute peripancreatic fluid collection


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


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

Etiology

• Alcohol

• Gallstone disease

• Hyperlipidaemy

• Hypercalcaemy

• Trauma

• Viral infectuions

• Idiopathic

• Ductal obstruction

– Tumour, diseases of the papilla

• Postoperative

• Iatrogenic

– ERCP

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

Complaints

• Pain

• Nausea, vomiting

• Tachycardia

• fever

• Swelling

• Paralytic ileus

• Hypotension, shock

• Renal failure

• Dyspnoe

• Coagulopathy (DIC)

• Cullen sign

• Grey-Turner sign

• Jaundice

• Sepsis

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.

Diagnosis II.

• Native chest and abdominal X-ray

• US

• CE-CT

• MR

• Leukocyta scintigraphy (if needed)

Diagnosis III.

Diagnosis IV.

Diagnosis V.

Diagnosis VI.

Mild acute pancreatitis

Non bacterial origin

Pathologic laesion (oedema)

Local „disease”

Recovery for conservative treatment (generally)

Mild acute pancreatitis

Conservative treatment

• „put the pancreas in rest”

• Gastric tube (suction)

• Ice/cold locally


• Intravenous fluids

• PPI

• Pain killers

• spamolithics

• EST

• Cholecystectomy

Severe acute pancreatitis

Non bacterial origin

Pathologic laesion (eg. necrosis)

In origin local than general disease

(SIRS, MODS/MOF )

Septic complications

(abscess)

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

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


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


Patomechanism

• Microcirculation theory– Local effect

• + NO and PAF increase the permeability of the small vessels, causes edema and decreases the microcirculation of the pancreas


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

Treatment I.

Konservative treatmentKonservative treatment

• ICU• Fluid and electrolyte resuscitation• Put the pancreas in rest• Painkillers, spasmolytics, EDA• Treatment of SIRS/MODS/MOF

Konservative treatment

• Fluid and elextrolyte resustitation (4-6000 ml/day)

• Blood gas correction

• Pain killers

• EDA

• Naso-gastric tube

• H2 blocker, PPI

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• Antibiotic prophylaxisAntibiotic prophylaxis imipenem/cilastatin 3x500 mg

• AB therapy

• Thoracocentesis

• Chest tube drainage

• Treatment of MODS Thrombosis prophylaxis

Treatment

Early enteral jejunal tube feedingEarly enteral jejunal tube feeding

• Scientific basis– Bowel mucosa atrophia– Bacterium translocation– CCK-PZ system– Disadventages of TPN

Naso-jejunal tube feedeing

• Within 48 hour insert the naso-jejunal feeding tube

• Next day start the feeding

• Increase the dosage of nutrients


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Naso-jejunal tube feedeing

• 25-30 kcal/kg/day (1500-2000 ml nutrien)

• Enteral pump

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

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

Percutaneous peripancreatic drainage

Acute peripancreatic fluid collections

• PPD

35%

• In 20% more than one drain


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• Becterium stain and resistency

• Lavage of the drains


• US observation

• Remove if the drained fluid is les than 20-30 ml/day and it is sterile

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

Surgery

Indication for surgeryIndication for surgery• Septic necrosis• Failure of PPD • Failure of conservative

treatment of MODS• Surgical complications

(perforation, bleeding, peritonitis)

• IAH/ACS


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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

Surgery

TecniqueTecnique

• Curved upper transversal laparotomy

• Blunt necrectomy• Exploration of retrocolic

spaces• Cholecystectomy + cystic

drain • Postoperative closed bursa

omentalis lavage

Surgery

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

The treatment of biliary pancreatitis

• EST is possible only in 70% of the cases

• Necrectomy, cholecystectomy and cystic duct drain

• Elective cholecystectomy

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acute pancreatitis szentkereszty zs. md. ph. d. med. habil. ud mhsc inst. surgery

Documents

sterile necrosis slide

fna slide

infected necrosis slide

surgery slide

atlanta classification

sex age ratio slide

retrocolic fluid

mild acute pancreatitis