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Presented by: Ahmad Pourhosseini common bile duct BODY TAIL HEAD pancreatic duct ampulla UNCINATE pancreatic enzymes PROTEOLYTIC ENZYMES Trypsinogen Chymotrypsinogen Proelastase Procarboxypeptidase A Procarboxypeptidase B AMYOLYTIC ENZYMES Amylase LIPOLYTIC ENZYMES Lipase Prophospholipase A2 Carboxylesterase lipase NUCLEASES Deoxyribonuclease (DNAse) Ribonuclease (RNAse) OTHERS Procolipase Trypsin 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 Idiopathic 10% Other 10% EtOH 35% Gallstones 45% Cholelithiasis Pancreas divisum Ethanol abuse Hereditary Idiopathic Hypercalcemia Medications Viral infections Hyperlipidemia Mumps ERCP Coxsackievirus Trauma End-stage renal failure Penetrating peptic ulcer AIDS therapy: didanosine, pentamidine Anti-inflammatory: sulindac, salicylates Antimicrobials: metronidazole, sulfonamides, tetracycline, nitrofurantoin Diuretics: furosemide, thiazides IBD: sulfasalazine, mesalamine Immunosuppressives: azathioprine, 6-mercaptopurine Neuropsychiatric: valproic acid Other: 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 defects CFTR SPINK1 acinar cell injury premature enzyme activation failed protective mechanisms premature enzyme activation autodigestion of pancreatic tissue local vascular insufficiency local complications activation of white blood cells release of enzymes into the circulation distant organ failure SEVERITY Mild STAGE 1: Pancreatic Injury Edema Inflammation STAGE 2: Local Effects Retroperitoneal edema Ileus STAGE 3: Systemic Complications Hypotension/shock Metabolic disturbances Sepsis/organ failure Severe Acute Pancreatitis Clinical Presentation Abdominal pain Epigastric Radiates to the back Worse in supine position Nausea and vomiting Fever Choledocholithiasis Perforated ulcer Mesenteric ischemia Intestinal obstruction Ectopic pregnancy Acute Pancreatitis Symptoms Diagnosis Abdominal pain Laboratory Elevated amylase or lipase > 3x upper limits of normal Radiology Abnormal sonogram or CT Grey Turner sign - flank discoloration due to retroperitoneal bleed in pt. with pancreatic necrosis (rare) Cullen’s sign - periumbilical discoloration (rare) Grey Turner sign Cullen’s sign Amylase Lipase ↑ Intestinal injury ↑ ↑ ↑ ↑ Tubo-ovarian disease ↑ Normal Renal failure ↑ ↑ ↑ Pancreatitis Parotitis Biliary stone Macroamylasemia Normal ↑ ↑ Normal EtOH: history Gallstones: abnormal LFTs & sonographic evidence of cholelithiasis Hyperlipidemia: lipemic serum, Tri>1,000 Hypercalcemia: elevated Ca Trauma: history Medications: history, temporal association Acute Pancreatitis Clinical Manifestations PANCREATIC PERIPANCREATIC Mild: edema, inflammation, fat necrosis Severe: phlegmon, necrosis, hemorrhage, infection, abscess, fluid collections Retroperitoneum, perirenal spaces, mesocolon, omentum, and mediastinum Adjacent viscera: ileus, obstruction, perforation SYSTEMIC Cardiovascular: hypotension Pulmonary: pleural effusions, ARDS Renal: acute tubular necrosis Hematologic: disseminated intravascular coag. Metabolic: hypocalcemia, hyperglycemia ER presentation 0 12 cytokine release 24 36 48 organ failure 60 hours from pain onset 72 84 96 Why are they needed? appropriate patient triage & therapy compare 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 Number Mortality <2 3-4 1% 16% 5-6 40% 7-8 100% appearance normal enlarged inflamed 1 fluid collection 2 or more collections grade A B C D E score 0 1 2 3 4 necrosis none < 33% 33-50% > 50% score 0 2 4 6 score morbidity mortality 1-2 4% 0% 7-10 92% 17% Balthazar et al. Radiology 1990. Scoring systems 3 Ranson criteria 8 APACHE II points 5 CT points Organ failure shock (SBP < 90 mmHg) pulmonary edema / ARDS (PaO2 < 60 mmHg) renal failure (Cr > 2.0 mg/dl) Local complications fluid collections pseudocysts necrosis (mortality 15% if sterile, 30-35% if infected) abscess Pancreatic rest Supportive care fluid resuscitation – watch BP and urine output pain control NG tubes and H2 blockers or PPIs are usually not helpful Refeeding (usually 3 to 7 days) bowel sounds present patient is hungry nearly 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) Abdominal pain with food aversion Nausea and vomiting Gastric atony Ileus Partial duodenal obstruction Mild Severe Pancreatitis Pancreatitis 80% 20% No Yes 80% 0% Morbidity 8% 38% Mortality 3% 27% Parameter Admissions Pancreatic necrosis Oral diet within 5 days 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.
