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G44 Gastroenterology
Pancreas
Toronto Notes 2019
When thinking about the causes of acute pancreatitis remember: I GET SMASHED, but vast majority due to gallstones or ethanol
Acute Pancreatitis
Etiology (most common are alcohol and gallstones)
• idiopathic:thoughttobehypertensivesphincterormicrolithiasis • gallstones(45%)
• ethanol(35%)
• tumours: pancreas, ampulla, choledochocele
• scorpionstings • microbiological
■ bacterial: Mycoplasma, Campylobacter, TB, M. avium intracellulare, Legionella, leptospirosis ■ viral: mumps, rubella, varicella, viral hepatitis, CMV, EBV, HIV, Coxsackie virus, echovirus,
adenovirus
■ parasites: ascariasis, clonorchiasis, echinococcosis
• autoimmune:SLE,polyarteritisnodosa(PAN),Crohn’sdisease • surgery/trauma
■ manipulation of sphincter of Oddi (e.g. ERCP), post-cardiac surgery, blunt trauma to abdomen, penetrating peptic ulcer
• hyperlipidemia(TG>11.3mmol/L;>1000mg/dL),hypercalcemia,hypothermia • emboliorischemia
• drugs/toxins
■ azathioprine, mercaptopurine, furosemide, estrogens, methyldopa, H2-blockers, valproic acid, antibiotics, acetaminophen, salicylates, methanol, organophosphates, steroids (controversial)
Pathophysiology
• activationofproteolyticenzymeswithinpancreaticcells,startingwithtrypsin,leadingtolocaland systemic inflammatory response
• ingallstonepancreatitis,thisisduetomechanicalobstructionofthepancreaticductbystones
• inethanol-relatedpancreatitis,pathogenesisisunknown
• inraregeneticdiseases,mutationspreventthephysiologicalbreakdownoftrypsinrequirednormally
to stop proteolysis (e.g. mutant trypsin in hereditary pancreatitis or mutation in SPINK 1 gene, which normally inhibits activated trypsin); may be model for ethanol-related pancreatitis
Pathology
• mild(interstitial)
■ peri-pancreatic fat necrosis ■ interstitial edema
• severe(necrotic)
■ extensive peri-pancreatic and intra-pancreatic fat necrosis
■ parenchymal necrosis and hemorrhage → infection in 60%
■ release of toxic factors into systemic circulation and peritoneal space (causes multi-organ failure)
• severityofclinicalfeaturesmaynotalwayscorrelatewithpathology • 3phases
■ local inflammation + necrosis → hypovolemia
■ systemic inflammation in multiple organs, especially in lungs, usually after IV fluids given →
pulmonary edema
■ local complications 2 wk after presentation → pancreatic sepsis/abscess
Signs and Symptoms
• pain:epigastric,noncolicky,constant • jaundice:compressionorobstructionofbileduct • canradiatetoback • Cullen’s/Grey-Turner’ssigns
• mayimprovewhenleaningforward(Inglefinger’ssign)• tetany:transienthypocalcemia
Gallstones only cause acute pancreatitis (not chronic pancreatitis)
Cullen’s Sign
Periumbilical ecchymosis
Grey-Turner’s Sign
Flank ecchymosis
Increased Amylase
• Sensitive, not specific
Increased Lipase
• Higher sensitivity and specificity • Stays elevated longer
• tenderrigidabdomen;guarding
• nausea/vomiting
• abdominaldistentionfromparalyticileus • fever:chemical,notduetoinfection
Investigations
• hypovolemicshock:canleadtorenalfailure • acuterespiratorydistresssyndrome
• coma
• increasedserumpancreaticenzymes:amylase,lipase(morespecific) • ALT>150specificforbiliarycause
• increasedWBC,glucose,lowcalcium
• imaging:CTmostusefulfordiagnosisandprognosis
■ x-ray: “sentinel loop” (dilated proximal jejunem), calcification, and “colon cut-off sign” (colonic spasm)
■ U/S: useful for evaluating biliary tree (67% sensitivity, 100% specificity)
■ CT scan with IV contrast: useful for diagnosis and prognosis because contrast seen only in viable
pancreatic tissue, non-viable areas can be biopsied percutaneously to differentiate sterile from
infected necrosis
■ ERCP or MRCP if cause uncertain, assess for duct stone, pancreatic or ampullary tumour, pancreas
divisum