Presented by: Ahmad Pourhosseini. pancreatic duct common bile duct ampulla pancreatic enzymes TAIL...
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Transcript of Presented by: Ahmad Pourhosseini. pancreatic duct common bile duct ampulla pancreatic enzymes TAIL...
pancreatic duct
common bileduct
ampulla
pancreatic enzymes
TAILTAIL
BODYBODY
HEADHEAD
UNCINATEUNCINATE
PROTEOLYTICPROTEOLYTIC LIPOLYTIC ENZYMESLIPOLYTIC ENZYMES ENZYMESENZYMES LipaseLipaseTrypsinogenTrypsinogen Prophospholipase A2Prophospholipase A2ChymotrypsinogenChymotrypsinogen Carboxylesterase lipaseCarboxylesterase lipaseProelastaseProelastaseProcarboxypeptidase AProcarboxypeptidase A NUCLEASESNUCLEASESProcarboxypeptidase BProcarboxypeptidase B Deoxyribonuclease (DNAse)Deoxyribonuclease (DNAse)
Ribonuclease (RNAse)Ribonuclease (RNAse)AMYOLYTIC ENZYMESAMYOLYTIC ENZYMESAmylaseAmylase OTHERSOTHERS
ProcolipaseProcolipaseTrypsin inhibitorTrypsin inhibitor
COMPARTMENTALIZATION - digestive enzymes are contained within zymogen granules in acinar cells
REMOTE ACTIVATION - digestive enzymes are secreted as inactive proenzymes within the pancreas
PROTEASE INHIBITORS – trypsin inhibitor is secreted along with the proenzymes to suppress any premature enzyme activation
AUTO “SHUT-OFF” – trypsin destroys trypsin in high concentrations
Acute inflammatory process involving the pancreas
Usually painful and self-limited Isolated event or a recurring illness Pancreatic function and morphology
return to normal after (or between) attacks
CholelithiasisEthanol abuse IdiopathicMedicationsHyperlipidemiaERCPTrauma
Pancreas divisumHereditaryHypercalcemiaViral infections
MumpsCoxsackievirus
End-stage renal failurePenetrating peptic ulcer
AIDS therapy: didanosine, pentamidineAnti-inflammatory: sulindac, salicylatesAntimicrobials: metronidazole, sulfonamides,
tetracycline, nitrofurantoinDiuretics: furosemide, thiazides IBD: sulfasalazine, mesalamine Immunosuppressives: azathioprine, 6-mercaptopurineNeuropsychiatric: valproic acidOther: calcium, estrogen, tamoxifen, ACE-I
Autosomal dominant with 80% phenotypic penetrance
Recurrent acute pancreatitis, chronic pancreatitis, and 50-fold increased risk of pancreatic cancer
Mutation in cationic trypsinogen gene (R122H)
Other genetic defectsCFTRSPINK1
autodigestion of pancreatic tissue
release ofenzymes intothe circulation
activationof white
blood cells
localcomplications
localvascular
insufficiency
premature enzyme activation
distantorgan failure
STAGE 1: Pancreatic InjuryEdemaInflammation
STAGE 2: Local EffectsRetroperitoneal edemaIleus
STAGE 3: Systemic ComplicationsHypotension/shockMetabolic disturbancesSepsis/organ failure
SEVERITYSEVERITYMildMild
SevereSevere
Abdominal painEpigastricRadiates to the backWorse in supine position
Nausea and vomitingFever
Acute PancreatitisAcute PancreatitisClinical PresentationClinical Presentation
SymptomsAbdominal pain
LaboratoryElevated amylase or lipase
> 3x upper limits of normal
RadiologyAbnormal sonogram or CT
Acute PancreatitisAcute PancreatitisDiagnosisDiagnosis
Grey Turner sign - flank discoloration due to retroperitoneal bleed in pt. with pancreatic necrosis (rare)
Cullen’s sign - periumbilical discoloration (rare)
AmylaseAmylase LipaseLipase
PancreatitisPancreatitis ↑↑ ↑↑
ParotitisParotitis ↑↑ NormalNormal
Biliary stoneBiliary stone ↑↑ ↑↑
Intestinal injuryIntestinal injury ↑↑ ↑↑Tubo-ovarian Tubo-ovarian
diseasedisease ↑↑ NormalNormal
Renal failureRenal failure ↑↑ ↑↑
MacroamylasemiaMacroamylasemia ↑↑ NormalNormal
EtOH: historyGallstones: abnormal LFTs & sonographic
evidence of cholelithiasisHyperlipidemia: lipemic serum, Tri>1,000Hypercalcemia: elevated CaTrauma: historyMedications: history, temporal association
Acute PancreatitisAcute PancreatitisClinical ManifestationsClinical Manifestations
PANCREATICPANCREATIC
PERIPANCREATICPERIPANCREATIC
SYSTEMICSYSTEMIC
Mild:Mild: edema, inflammation, fat necrosis edema, inflammation, fat necrosisSevere:Severe: phlegmon, necrosis, hemorrhage, phlegmon, necrosis, hemorrhage, infection, abscess, fluid collectionsinfection, abscess, fluid collections
Retroperitoneum, perirenal spaces, mesocolon, Retroperitoneum, perirenal spaces, mesocolon, omentum, and mediastinumomentum, and mediastinum
Adjacent viscera:Adjacent viscera: ileus, obstruction, perforation ileus, obstruction, perforation
Cardiovascular:Cardiovascular: hypotension hypotensionPulmonary:Pulmonary: pleural effusions, ARDS pleural effusions, ARDSRenal:Renal: acute tubular necrosis acute tubular necrosisHematologic:Hematologic: disseminated intravascular coag. disseminated intravascular coag.Metabolic:Metabolic: hypocalcemia, hyperglycemia hypocalcemia, hyperglycemia
Why are they needed?appropriate patient triage & therapycompare results of studies of the impact of
therapy When are they needed?
optimally, within first 24 hours (damage control must begin early)
Which is best?
Ranson Criteria (1974) based on clinical & laboratory parameters scored in first 24-48 hours of admission poor positive predictors (better negative predictors)
APACHE Scoring System can yield a score in first 24 hours APACHE II suffers from poor positive predictive value APACHE III is better at mortality prediction at > 24
hours Computed Tomography Severity Index
much better diagnostic and predictive tool optimally useful at 48-96 hours after symptom onset
appearanceappearance normalnormal enlargedenlarged inflamedinflamed 1 fluid 1 fluid collectioncollection
2 or more 2 or more collectionscollections
gradegrade AA BB CC DD EE
scorescore 00 11 22 33 44
necrosisnecrosis nonenone < 33%< 33% 33-50%33-50% > 50%> 50%
scorescore 00 22 44 66
scorescore morbiditymorbidity mortalitymortality
1-21-2 4%4% 0%0%
7-107-10 92%92% 17%17%
Balthazar et al. Radiology 1990.Balthazar et al. Radiology 1990.
Scoring systems 3 Ranson criteria 8 APACHE II points 5 CT points
Organ 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)abscess
Pancreatic rest Supportive care
fluid resuscitation – watch BP and urine output
pain controlNG tubes and H2 blockers or PPIs are
usually not helpful Refeeding (usually 3 to 7 days)
bowel sounds presentpatient is hungrynearly pain-free (off IV narcotics)amylase & lipase not very useful here
Pancreatic rest & supportive care fluid resuscitation* – may require 5-10 liters/day careful pulmonary & renal monitoring – ICU maintain hematocrit of 26-30% pain control – PCA pump correct electrolyte derangements (K+, Ca++, Mg++)
Rule-out necrosis contrasted CT scan at 48-72 hours prophylactic antibiotics if present surgical debridement if infected
Nutritional support may be NPO for weeks TPN vs. enteral support (TEN)
ParameterParameterMildMild
PancreatitisPancreatitis
SevereSevere
PancreatitisPancreatitis
AdmissionsAdmissions 80%80% 20%20%
Pancreatic Pancreatic necrosisnecrosis NoNo YesYes
Oral diet within 5 Oral diet within 5 daysdays 80%80% 0%0%
MorbidityMorbidity 8%8% 38%38%
MortalityMortality 3%3% 27%27%
Acute pancreatitis is a self-limited disease in which most cases are mild.
Gallstones and alcohol are the leading causes of acute pancreatitis.
In mild pancreatitis, nutritional support is usually not required
In severe pancreatitis, nutritional support will likely be required with the enteral route preferred over TPN because of both safety and cost.