microscopic view of pancreatic acini pancreatic duct duodenum

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Acute appendicitis

Acute pancreatitisChair of faculty surgery # 2 First Moscow State Medical University

Natroshvili A.G.Anatomy and physiologydigestive enzymeshormones

microscopic viewof pancreatic acini

pancreatic ductduodenumAnatomy and physiologytrypsinogentrypsinchymotrypsinelastasephospholipasecarboxypeptidaseenterokinasechymotrypsinogenproelastaseprophospholipaseprocarboxypeptidaseduodenal lumenNormal Enzyme ActivationAnatomy and physiologyExocrine StimulationThe more proximal the nutrient infusionthe greater the pancreatic stimulation (dog studies)stomach maximal stimulationduodenum intermediate stimulationjejunum minimal / negligible stimulationElemental formulas tend to cause less stimulation than standard intact formulasintact protein > oligopeptides > free amino acidsIntravenous nutrients (even lipids) do not appear to stimulate the pancreasAnatomy and physiologyProtectionCOMPARTMENTALIZATION - digestive enzymes are contained within zymogen granules in acinar cellsREMOTE ACTIVATION - digestive enzymes are secreted as inactive proenzymes within the pancreasPROTEASE INHIBITORS trypsin inhibitor is secreted along with the proenzymes to suppress any premature enzyme activationAUTO SHUT-OFF trypsin destroys trypsin in high concentrationsAcute pancreatitisDefinitionAcute inflammatory process involving the pancreasUsually painful and self-limitedIsolated event or a recurring illnessPancreatic function and morphology return to normal after (or between) attacks

Acute pancreatitisEtiologyAcute pancreatitisAssociated conditionsCholelithiasisEthanol abuseIdiopathicMedicationsHyperlipidemiaERCPTraumaEnd-stage renal failurePenetrating peptic ulcer

Acute pancreatitisPathogenesisAcinar cell injuryPremature enzyme activationFailed protective mechanismsAudodigestion of pancreatic tissueLocal vascular insufficiencyActivation of white blood cellsRelease of enzymes into the circulationLocal complicationsDistant organ failureAcute pancreatitisPathogenesisSTAGE 1: Pancreatic InjuryEdemaInflammationSTAGE 2: Local EffectsRetroperitoneal edemaIleusSTAGE 3: Systemic ComplicationsHypotension/shockMetabolic disturbancesSepsis/organ failureSEVERITYMild

SevereMild AP (no necrosis) 0%Sterile necrosis 10%Infected necrosis 25%

Acute pancreatitis11 Since majority of the patients with mild acute pancreatitis recover without any short term complications or long term sequelae. So majority of the studies have focussed on management of acute necrotizing pancreatitis. I would also Acute pancreatitisClinical presentationAbdominal painEpigastricRadiates to the back (belt painWorse in supine positionNausea and vomitingFeverLaboratoryElevated amylase or lipase > 3x upper limits of normalLipase has slightly higher sensitivity and specificity and greater overall accuracy than amylase (Evidence category A)RadiologyAbnormal sonogram or CT

Differential DiagnosisCholedocholithiasisPerforated ulcerMesenteric ischemiaIntestinal obstructionEctopic pregnancyAcute pancreatitisClinical presentationMild: edema, inflammation, fat necrosisSevere: phlegmon, necrosis, hemorrhage, infection, abscess, fluid collections

Retroperitoneum, perirenal spaces, mesocolon, omentum, and mediastinum

Adjacent viscera: ileus, obstruction, perforation

Cardiovascular: hypotensionPulmonary: pleural effusions, ARDSRenal: acute tubular necrosisHematologic: disseminated intravascular coag.Metabolic: hypocalcemia, hyperglycemiaPANCREATIC

PERIPANCREATIC

SYSTEMICAcute pancreatitisPredictors of severityWhy are they needed?appropriate patient therapycompare results of studies of the impact of therapyWhen are they needed?optimally, within first 24 hours (damage control must begin early)Which is best?Acute pancreatitisScoring systemsRanson and Glasgow Criteria (1974)based on clinical & laboratory parametersscored in first 24-48 hours of admissionpoor positive predictors (better negative predictors)APACHE Scoring Systemcan yield a score in first 24 hoursAPACHE II suffers from poor positive predictive valueAPACHE III is better at mortality prediction at > 24 hoursComputed Tomography Severity Indexmuch better diagnostic and predictive tooloptimally useful at 48-96 hours after symptom onsetAcute pancreatitisScoring systems: Ranson criteria for alcoholic pancreatitisAT ADMISSIONAge > 55 yearsWBC > 16,000Glucose > 200LDH > 350 IU/LAST > 250 IU/L

WITHIN 48 HOURSHCT drop > 10BUN > 5Arterial PO2 < 60 mm HgBase deficit > 4 mEq/LSerum Ca < 8Fluid sequestration > 6LNumberMortality 50%score0246scoremorbiditymortality1-24%0%7-1092%17%Balthazar et al. Radiology 1990.Acute pancreatitisSevere pancreatitisScoring systems 3 Ranson criteria 8 APACHE II points 5 CT pointsOrgan failureshock (SBP < 90 mmHg)pulmonary edema / ARDS (PaO2 < 60 mmHg)renal failure (Cr > 2.0 mg/dl)Local complicationsfluid collections pseudocystsnecrosis (mortality 15% if sterile, 30-35% if infected)abscessAcute pancreatitisAdditional diagnostic tests: UltrasonographyLittle part in the diagnosis of the acute pancreatitis due to bowel dilatationMain signs: enlarged hypoechogenic pancreas, possible fluid collectionsRole in biliary pancreatitis Stones in gallbladderCommon Bile Duct dilation US findings should be examined in all patients with possible acute pancreatitis on admission (Evidence category B)

Acute pancreatitisAdditional diagnostic tests: CT-scanHighly informativeNormal Homogeneous enhancement of the whole pancreasAbnormal Non-visualization of a part of the pancreasSensitivity of 90-95%Specificity 100%

Routine use of CT scan within 24-48 hours of admission (Evidence category C) A dynamic CT scan should be performed in all (predicted) severe cases between 3 and 10 days after admission (Evidence category B)

Acute pancreatitisAdditional diagnostic lab testsAmylase and lipasePlasma level peak within 24 hourst1/2 of amylase 80% of deathsIntestinal floraGram negative bacteria Mechanism translocation of the bacteria across the gut wallProphylactic antibacterial treatment is strongly recommended in severe pancreatitis (Evidence B)No evidence when to start prophylactic treatment or how long to continue therapyAppropriate antibiotics are those that are active against in particular gram-negative organismsCommence as early as possible after the identification of a severe attack Acute pancreatitisPancreatic necrosisSterile necrosis Systemic Inflammatory Response Syndrome (SIRS) (First week)Mortality rate of 10-40%Sterile pancreatic necrosis surgery in selected casesSelected cases Massive pancreatic necrosis (>50%) with a deteriorating clinical course (Evidence C)Patients with progression of organ dysfunctionNo signs of the improvement (grade B)Acute pancreatitisPancreatic necrosisInfected necrosis Sepsis (After 3 weeks)Mortality 20-70%US or CT guided FNA with gram stain and culture is a confirmatory test (Evidence A)Suspect if: Exacerbation of clinical signsLaboratory blood test changesShift to immature cellsElevation of CRPIncreased APACHE IIPositive blood cultureNecrosectomy is indicated in a confirmed infected pancreatic necrosis (Evidence A)

Acute pancreatitisPancreatic necrosisInfected necrosis Sepsis (After 3 weeks)Mortality 20-70%US or CT guided FNA with gram stain and culture is a confirmatory test (Evidence A)Suspect if: Exacerbation of clinical signsLaboratory blood test changesShift to immature cellsElevation of CRPIncreased APACHE IIPositive blood cultureNecrosectomy is indicated in a confirmed infected pancreatic necrosis (Evidence A)

Acute pancreatitisAlgorithmConfirm acute pancreatitisAmylase/LipaseTrypsinogetn2CT scan in atypical casesInitial managementSeverity stratification

IV fluid/pain conrolScoring systemsC-reactive proteinMild acute pancreatitisSevere acute pancreatitisAcute pancreatitisAlgorithmMild acute pancreatitisSevere acute pancreatitisRECOMMENDEDAdmit to general wardRefeed when pain subsidesNOT RECOMMENDEDAntibioticsCT scan

RECOMMENDEDAdmit to ICUAntibioticsCT-scan day 3NECROSISSterile observe (CT, US)Infection suspected fine needle aspiration/drainage under US or CT controlInfected necrosis necrosectomyOpen drainage of abscesses, retroperitoneal space