Acute Pancreatitis - Prof.Dr.Ömer Şentürkdromersenturk.com/.../Acute-Pancreatitis.pdf1 Acute...
Transcript of Acute Pancreatitis - Prof.Dr.Ömer Şentürkdromersenturk.com/.../Acute-Pancreatitis.pdf1 Acute...
1
Acute Pancreatitis
Prof. Dr. Ömer ŞENTÜRK
Presentation Plan1. Anatomy2. Acute pancreatitis definition3. Epidemiyology4. Etiology5. Pathogenesis6. Clinical findings7. Laboratory findings8. Radiological findings9. Differential diagnosis10. Complications 11. Treatment12. Prognosis13. Oddi sphincter dysfunction
Dr.Ö.Ş
Acute Pancreatitis
The revised Atlanta classification requires that two or more of the
following criteria be met for the diagnosis of acute pancreatitis:
(a) abdominal pain suggestive of pancreatitis,
(b) serum amylase or lipase level greater than three times the upper
normal value, or
(c) characteristic imaging findings
There should be no structural changes to the pancreas duct in the stone or pancreas to suggest chronic pancreatitis.
Dr.Ö.Ş
Acute Pancreatitis and Imaging Modality
Many patients will meet the criteria for acute pancreatitis on the
basis of symptoms and laboratory results alone and may not require
imaging initially,
Imaging may be performed;1- early in the disease course when the cause of the disease is
unclear
2- to look for causative factors such as choledocholithiasis and
pancreatic cancer
3- when abdominal pain suggests pancreatitis but the amylase or
lipase level is not elevated to the threshold value, which is often the
case at delayed presentation.
Dr.Ö.Ş
Epidemiyology
Variability of clinical course ...Different countries in different frequencyIn Turkey?Increased incidence in recent years…l Advances and developments in diagnosis…l Increase in alcohol usel Increase in cholelithiasis frequency
M/F = 1/1Alcoholic pancreatitis is more common in young menDiseases of the gallbladder and biliary tract are more common in older women...
Dr.Ö.Ş
Etiology • Metabolic diseases• Hypertriglyceridemia• Hypercalcemia• Renal failure
• Operations• ERCP• Pancreas trauma• Drugs and toxic substances• Pregnancy• Penetrating peptic ulcer• Pancreas ca• Pancreatic divisum• Hereditary pancreatitis• Scorpion sting• Infections
• Hepatitis A B C,• Mumps, • Coxsackie virus...
• Collagen tissue diseases•SLE, PAN...
Others
Biliary
Alcohol
İdiopathic
Dr.Ö.Ş
2
EtiologyFree fatty acids can cause acute pancreatitis by damaging pancreatic acinar cells and capillary endotheliumTypically three types of patients develop pancreatitis due to hypertriglyceridemia;l Patients with alcoholic + hypertriglyceridemial Patients with poorly controlled diabetes + hypertriglyceridemial Patients without diabetes and obesity who develop hypertriglyceridemia due to
medication or diet Complaints of patients presenting with pancreatitis due to hypertriglyceridemia are similar to others, but amylase levels are not as high as expectedCalcium leads to acute pancreatitis by precipitating into the pancreatic duct and causing trypsinogen activation
Dr.Ö.Ş
Etiology
Possible causes of idiopathic acute pancreatitis (It is seen in between10-30%)
Hidden gallstone disease (USG negative)
Unrecognized hypertriglyceridemia
Pancreas ca
Abnormalities of bile and pancreatic duct
Oddi sifincter dysfunction
Cystic fibrosis
Drugs…
Dr.Ö.Ş
Pathogenesis
Blockage of the pancreatic duct
Blockage of biliopancreatic duct
Oddi sphincter dysfunction (reflux of duodenal content)
Dr.Ö.Ş
Risk Factors in the Development of Gallstone-Induced Pancreatitis
High RiskBroadVerySmall
Low RiskNarrowLittleBig
Diameter of cystic channelNumber of stonesDiameter of the stones
Dr.Ö.Ş
FrequentAsparaginaseAzathiopurine6-mercaptopurineDidanosinePentamidinValproate
RareACE inh.Acetaminophen5-ASAFurosemideSulfosalazineThiazideOctreotide
Quite RareCarbamazepineCorticosteroidsEstrogensMinocyclineNitrofurantoinTetracyclineMetronidazole
Drugs That Cause Acute Pancreatitis:
Dr.Ö.Ş
ImmunologicAminosalicylatesSulfonamids 6-mercaptopurine
Direct toxicDiureticsSulfonamids
Toxic metaboliteValproic acidsDidanozinePentamidineTetracycline
Leading to ischemiaDiureticsAzathiopurine
Caused increased viscosity in pancreatic fluid
DiureticsSteroids
Drugs That Cause Acute Pancreatitis:
Dr.Ö.Ş
3
Pancreatitis Due To ERCP: Risk FactorsPatientsExact
WomanOddi sphincter dysfunctionHistory of pancreatitis
LikelyYoung ageNon-dilated EHBDAbsence of chronic pancreatitisNormal serum B levels
OperationExact
Precut sphincterotomyPancreatic injections
LikelyDifficult cannulationSphincter dilatation with biliary balloonPancreatic sphinctrotomyFailure of the stones in the bile duct
Frequency %0,2-25Dr.Ö.Ş
Prevention of Pancreatitis Due To ERCP
• Avoid unnecessary ERCP (MRCP, EUS)• Indomethacin supp before treatment• Pancreatic stent after papillatomy• Gabexate• Somatostatin
Dr.Ö.Ş
(Vacuol)Trypsinogen
Cathepsin B
Trypsinogen activator peptide
Wirsung Channel
Obstruction
Rupture of vacuoles
Trypsinogen Activation
Increased trypsin production
Active trypsin secretion
Pathogenesis
Autodigesion of
pancreas
Excessive increase in trypsin production
Increase in other pancreatic enzymes(phospholipase, chymotripsin, elastase)
Increase in other digestive enzyme cascade
(Complement cascade, kallikrein-quinine,
coagulation and fibrinolysis
Dr.Ö.Ş
Intraparenchymal tryipsin
activation
Elastase
Complement factors
Kallikrein
Chymotripsin Lipase
Thrombin
PhospholipaseA 2
Damage toblood
vessels
Leucotaxis
Increased permiability in
capillaries and veins
Capillary damage
Fatnecrosis
AcuteDIC
AlveolerCell
mambrane damage
Enzyme effects
Dr.Ö.Ş
Clinical FindingsAbdominal painNausea-vomitingFeverTachycardia, hypotensionMeteorism, ileus, subileusIcterMetabolic disordersl Hypocalcemil Hyperglisemil Met.acidosis
Pancreatic ascitesNeurological findingsPleural effusionCullen,Grey Turner and Fox Organ failurel ARDSl Renal failurel DIC and C-V failure
Dr.Ö.Ş
4
Laboratory FindingsAmylase and lipasel Hyperamylasemial Macroamylasemia
Hematological and biochemical testsl Leukocytosis, elevated AST, ALT, GGT, ALP and Bl a-2 macroglobulinl Polymorpho nuclear elastasel CRPl BUN, Cr, albumin, Ca, P, glucose, blood gases...
Peritoneal fluid aspiration
0
2
4
6
8
10
12
0 6 12 24 48 72 96
AmilazLipaz
Saat
Incr
ease
in m
ultip
les
of n
orm
al
Dr.Ö.Ş
Amylase…Nonspecific !!!l Amylase > 3x normal à Consider pancreatitis !…
l May be normal in chronic pancreatitis !...l Enzyme level ¹ Severityl False (-): acute attack on chronic alcohol intake; HyperTGl False (+): kidney failure, acidemia…
Lipasel More sensitive and spesific than amylase
Laboratory Findings
Dr.Ö.Ş
Causes of Elevated Serum Amylase
Pancreatitis CholesystitCholangitisPeptic ulcerNephrolithiasisIntestinal obstruction, ischemia, perforationEctopic pregnancy……
Dr.Ö.Ş
Radiological FindingsDirect Abdominal X-Ray
l Air in duodenal ans
l Sentinel loop sign (expanded jejunal ans)
l Colon cut-off sign
l Calcifications in the pancreas region
Chest X-Ray
Abdominal USG
Abdominal BT
l Balthazar
Abdominal MR
ERCP
MRCP
Dr.Ö.Ş
Gastric gas
Small bowel gas
Rectum/Sigmoid gas
Normal Gas Pattern
Sırt üstü
Dr.Ö.Ş
Sentinel Loop
Sırt üstü Yüz üstü
Dr.Ö.Ş
5
Colon cut-off sign
Dr.Ö.Ş26
CT’nin Amacı• Prognosis• CT staging • Evaluation of complications • Guide biopsy or aspiration
CT: Normal Pancreas
Dr.Ö.Ş
CT: Acute Pancreatitis
Dr.Ö.Ş
CT:Necrotizing Pancreatitis
Dr.Ö.Ş
Differential Diagnosis
Peptic ulser disese (penetration-perforation)
Acute cholesystitIntestinal obstructionMesenteric ischemiaMesenteric vascular trom.PeritonitOver ca
SalphengitisPneumoniaMyokardial infarctionUreter stonesDiverticulitisColon perforationAbdominal aortic aneurysm rupture
Dr.Ö.Ş
Complications
Local Complicationsl Pseudocystsl Abscessl Pancreatic fistulal Fluid collectionl Necrosisl Pancreatic hemorrhagel GIS bleedingl Colon obstruction
Systemic Complicationsl Shockl ARFl ARDSl Pleural effusionl Atelectasisl C-V failurel Metabolic disturbance...l DİCl Metastatic fat necrosisl Encephalopathy
Dr.Ö.Ş
6
LungPleural effusion
AtelectasisARDS
PneumoniaShock lung
C-VHypvolemia
ShockHyperdynamic
circulation
CoagulationDIC
RareSubcutaneous fat
necrosisArthritis
RhabdomyolysisOsteolyzis
BrainEncephalopathy
MetabolicHypocalcemiaHyperglisemiaHypokalemia
Hypoalbuminemi
KidneyOliguriaAnuria
CardiacPericardial effusion
Arrhytmia
Systemic Complications
Dr.Ö.Ş
Treatment
Medical Treatmentl Supportive treatment...l Reduction of inflammation...l Diagnosis and treatment of complications...
Surgery Treatment
Dr.Ö.Ş
TreatmentSupportive Treatment
General Approach
Oral intake is stopped
İV fluid...
Correction of acid
base and electrolyte
balance...
Analgesic for pain...
TPN ?
NG tube
Medication
Antichollinergics
H-2 RA, PPI
Glucagon
Calsitonin
Somotostatin and
Octreotide
Dr.Ö.Ş
TreatmentNG Tube
l Endicationsl Persistent vomitingl Obstruction
Does not change the course of the disease !..
Dr.Ö.Ş
TreatmentEmergency Sphincterotomy and Stone Extraction
• Severe pancreatitis• Cholangitis / Icter
Dr.Ö.Ş
TreatmentReduction of Inflammation
Aprotinin (proteas inhibitor)
Gabexate (proteas and fosfolipase A-2 inhibitor)
Fresh frozen plasma
Factors that activate monocyte and macrophage system
Antioxidants (selenium, A,C,E vit., metionin, acetylcysteine)
Lexipafant (PAF antagonist)
Dr.Ö.Ş
7
Locall Necrosis
l Sterile à Observation, debridement, prophylactic ABl Infected à Debridement, necrosectomy, AB use
l Pseudocyts à Observation, endoscopic or surgical treatmentl Abscess à Surgical drainagel GIS bleeding
l Erosive gastritis à PPIl Gastric varices à Sclerotherapy / Surgeryl Pseudoanev. ruptur à Embolisation / Surgery
Systemic
TreatmentTreatment of Complications
Dr.Ö.Ş
Pseudocysts: Treatment
AspirationInternal drainageEksternal drainageTrans-papiller drainage
Dr.Ö.Ş
Prophylactic AntibioticsIn which case à Severe diseaseIn which antibiotics à Broad spectrum
Antibiotic penetrating the pancreas When à Early period of disease How long (time) à 14-28 days
Dr.Ö.Ş
TreatmentTreatment of Complications
Systemicl Hypocalcemia... Ca replacementl Hyperglisemia… Insulin treatmentl Respiratory failure... Oxygen treatmentl ARDS..... Mechanical ventilationl ARF... Hemodialysisl DIC..... Fresh frozen plasma, heparinl Shock... Correction of asid base and
electrolyte balance, dopamine...
Dr.Ö.Ş
Treatment ERCP
Suspicion of gallstone pancreatitis;l Elevation of LFT (especially ALT ≥3xN) l Determination of stone in gallbladder andl Detection of biliary tract dilatation in USG and other
radiological examinations
Dr.Ö.Ş
Treatment ERCP
Emergency ERCP (within the first 24 hours);l Severe biliary pancreatitis associated with stonel Cholangitis
Dr.Ö.Ş
8
Treatment ERCP
Indications of ERCP;l Removal of bile duct stones in patients with severe
pancreatitisl Patients with cholangitisl Patients not eligible for cholecystectomyl Postcholecystectomyl In the presence of strong evidence of biliary obstruction
Dr.Ö.Ş
Treatment ERCP
Routine ERCP should be avoided;l Patients with low suspicion of bile duct stonesl All patients scheduled for cholecystectomy
“Routine precholecystectomy ERCP is not recommended in patients with
billiary pancreatitis…”
Dr.Ö.Ş
PrognosisBed head assesmentl Evaluates the severity of the disease less than it is
Scoring systeml Ranson, Glasgow, Apache, Rabenek
Serum markersl Trypsinogen activating peptide (TAP)l CRPl Cytokines (IL-6)l Polymorpho nuclear elastasel Phospholipase A-2l a-2 macroglobulin
CT criterionl Liquid accumulation, necrosis
Dr.Ö.Ş
Ranson Criteria(Non-biliary Pancreatitis)
On first arrivalAge> 55 yearsWBC > 16.000 mm3
Glucose > 200mg/dlLDH > 350 IU/LAST > 120
48 hours laterReduction in Hct > %10Increase in BUN > 5mg/dlSerum Ca <8 mg/dlArterial PaO2 < 60 mmHgBase deficient > 4 mEq/LFluid gap > 6 L
Dr.Ö.Ş
Ranson Criteria(Biliary Pancreatitis)
On first arrivalAge> 70 yearsWBC > 18.000 mm3
Glucose > 220mg/dlLDH > 400 IU/LAST > 250 IU/L
48 hours laterReduction in Hct > %10 Increase in BUN > 5mg/dlSerum Ca <8 mg/dlArterial PaO2 < 60 mmHgBase deficient > 4 mEq/LFluid gap > 6 L
Dr.Ö.Ş
0
20
40
60
80
0-2 38475 38570 386650-2 3-5 6-8 9-11
According to Ranson Criteria Risk Factors: Mortality
% Mortality
ScoreDr.Ö.Ş
9
Determination of Severity with CT: Balthazar Index
CT findings PointPankreatic growth 1Peripancreatic inflammation 2Fluid collection in only one area 3Fluid collection in more than one area 4Necrosis <%30 2Necrosis %30-50 4Necrosis >%50 6
DiagnosisPrognosisDetection of complications
Dr.Ö.Ş
85% Light-edematous formNo organ failure outside the pancreas
15% Severe necrotizing pancreatitisOne or more organ failure.
1% MortalityTransient disruption of exocrine and endocrine functionsSequel: Pseudocysts (rare)
10-20% Mortality Exocrine and endocrine function transient deterioration, in severecases permanent detrioration Sequel:Pseudocysts, pancreatic abscess, Colon necrosis
Prognosis
Dr.Ö.Ş
Oddi Sphincter Dysfunction
Benign, stone-free obstructive diseasel Pancreaticobilier type pain,l Cholestasis and/orl Causes pancreatitis
Clinic;l Middle age woman l It is the first one to respond to cholecystectomy and then again to have
no pain l Pain in the right upper quadrant, epigastrium and spread on the back l Continuous or episodic painl Nausea-vomiting
Dr.Ö.Ş
Diagnosis ;l Slight increase in serum LFT (< X2)l Morphine/prostigmin provocation test
l Pain + ALT, AST, AP, AMİLAZ, LİPAZ in case of 4-fold increase in enzymes à Test positive
l USG l After lipid rich meal eat or CCK administration expansion pancreatic duct
l Biliary scintigraphyl Cholangiographyl Manometry
Oddi Sphincter Dysfunction
Dr.Ö.Ş
Milwauke classificationl Biliary I
l Biliary type painl AST/AP > 2xNormall The ERCP contrast agent drains over 45 minutesl Common bile duct > 12 mm
l Biliary IIl Biliary type painl There are 1 or 2 other features
l Biliary IIIl Only biliary type pain
Oddi Sphincter Dysfunction
Dr.Ö.Ş