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Pancreatic and Biliary Disease: An Overview

Tory Davis PA-C. Pancreatic and Biliary Disease: An Overview. Table of Contents. Pancreatic disease Acute pancreatitis Chronic pancreatitis Gallbladder disease Cholelithiasis Cholecystitis. Acute Pancreatitis. Inflammation of pancreas (+/-adjacent tissue)

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Pancreatic and Biliary Disease: An Overview

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  1. Tory Davis PA-C Pancreatic and Biliary Disease: An Overview

  2. Table of Contents Pancreatic disease Acute pancreatitis Chronic pancreatitis Gallbladder disease Cholelithiasis Cholecystitis

  3. Acute Pancreatitis Inflammation of pancreas (+/-adjacent tissue) caused by release of activated pancreatic enzymes within gland (autodigestion) Several possible etiologies Range from mild (abd pain, vomiting- inflammation confined to gland, 5% mortality) to severe (really bad, maybe dead: pancreatic necrosis, systemic inflammatory process, shock, multi-organ failure- up to 50% mortality)‏

  4. What’s happening Pancreatic enzymes (trypsin, phospholipase A2, elastase) get activated within the gland Cause tissue damage directly AND Activate complement and inflammatory cascades, producing cytokinesinflammation, edema, tissue necrosis

  5. Then what? Cytokines and enzymes in peritoneum cause chemical burns, fluid third-spacing In systemic circ systemic inflammatory responsecapillary permeability and  vascular tone acute respiratory distress, renal failure

  6. Who’s responsible for this mess? EtOH- 100 g/d x 3-5 yrs (lots)pancreatic enzyme proteins to precipitate in small ductulesobstructionpremature activation of enzymes Biliary/structural- gallstone in Sphincter of Oddi ductal pressures

  7. Etiology 80% caused by alcohol or biliary tract disease/structural disorders Stones ERCP (dx imaging study) Trauma Ischemia Vasculitis Pancreas divisum – predisposes for pancreatitis

  8. Etiology 20% caused by “other” Drugs: ACE-I, sulfa, NSAIDs Infectious: CMV, mumps, Coxsackie B Inherited: CF, other gene mutations Metabolic: hypertrigs, hypercalcemia, hyperparathyroid Other: pregnancy, embolism

  9. Causes of Acute Pancreatitis: GET SMASH'D Gallstones (most common reason for acute pancreatitis with amylase >1000 units/L)‏ Ethanol (alcohol)‏ Trauma (usually blunt abdominal injury)‏ Steroids Mumps Autoimmune Scorpion bites (akin to zebra bites in Maine)‏ Hyperlipidemia (particularly hypertriglyceridemia)‏ Drugs (ACE-I, sulfa)‏

  10. Acute Pancreatitis S&S Steady, boring deep epigastric pain Radiates to the back in 50% Sudden onset with gallstone pancreatitis, gradual sx increase over days with EtOH Nausea and vomiting common Alleviated by sitting upright, lean forward Aggravated by vigorous movement, deep inspiration, coughing Weakness, anxiety, diaphoresis

  11. Physical Exam Acutely ill appearing Febrile Mild jaundice possible Tachycardic, diaphoretic, pale Tachypneic with shallow respirations  diaphragmatic excursion Why? Don’t want to breath Postural hypotension Blunted sensorium

  12. Exam Marked upper and mild lower abd tenderness with guarding Mild-moderate upper abd rigidity Rectum nontender, neg FOBT Hypoactive BS, maybe absent (ileus)‏ Evidence of extravasation of hemorrhagic exudate Grey Turner’s sign: flank ecchymosis Cullen’s sign: umbilical ecchymosis

  13. Work-up Lipase more specific, elevated up to 14 days Amylase elevate early, recedes 3-5 days Non-specific to pancreas CMP- elevated glucose, Ca elevated alk phos and bilirubin indicating obstruction LDH- elevated from tissue necrosis

  14. Work-up CBC with diff- WBC up to 12-20 Hct 50-55% (indicating 3rd spacing)‏ EKG- r/o MI U/S to image biliary tree Start here - it’s faster and cheaper Stones easily observable and fixable CT to image pancreas itself Necrosis, vascular involvement, mass

  15. Ddx Perforated ulcer (gastric, duodenal)‏ Mesenteric infarction Strangulating intestinal obstruction Dissecting aneurysm Biliary colic Appendicitis Inferior wall MI Splenic hematoma Abd muscle hematoma

  16. Ranson’s Criteria for Pancreatitis Mortality Determine and document at admission Age >55 Glucose>200 Serum LDH>350 AST>250 WBC>16,000 If 3 or more present at admission, severe course predicted with 60-80% sensitivity

  17. Ranson’s Criteria: Part 2 Development of these in 1st 48h heralds worsening prognosis HCT  > 10% BUN  > 5mg/dL Ca <8mg/dL PaO2 <60 mmHg Fluid sequestration >6L Base deficit over 4 meq/L

  18. Ranson’s CriteriaMortality proportional to # of criteriaDownload to your PDA for IM rotations… Number of Criteria 0-2 3-4 5-6 7-8 Mortality 1% 16% 40% 100%

  19. Treatment Adequate fluids- up to 6-8 L/day IV fluid with lytes- dilute enzymes, reduce inflammatory markers NPO until acute inflammation subsides To avoid stimulation or release of enzymes Until pain/tenderness resolved, nl labs, appetite present, feels better- may take days to weeks NG tube for pts with ileus, abd distention, vomiting

  20. Acute pancreatitis Tx Pain relief- parenteral opioids such as demerol Anti-emetics H2 blockers and/or PPI why? Stop stomach acid production (doesn’t stimulate pancreas) IVF Surgical consult for severe pancreatitis

  21. Treatment ICU admission if oliguric, hypotensive, Ranson’s  3, or pancreatic necrosis by CT >30% Humidified O2 if hypoxic Treat heart failure, renal failure, hyperglycemia, hypomagnesemia etc Abx (imipemem x 1 wk)‏

  22. Tx If gallstone pancreatitis: 80% will pass stone spontaneously within 24h If not…ERCP w/ sphincterotomy and stone removal If they DO pass the stone spontaneously, may elect lap cholecystectomy later

  23. Oh and.. After 5-7d, necrotic tissue can become infected If pt initially stabilizes, then deteriorates OR if pt appears toxic, w/ high temp, high WBCs, suspect infection with enteric bacteria 100% mortality unless aggressive tx with surgical debridement or drainage

  24. Other complications Intravascular volume depletion, shock Prerenal azotemia May require peritoneal or hemodialysis ARDS- acute respiratory distress syndrome Pancreatic abscess- needs drainage GI bleed

  25. Chronic Pancreatitis Persistent inflammation of pancreas permanent structural damage  decrease in endocrine and exocrine functions

  26. Chronic Pancreatitis In US, 70-80% from alcohol, 15-25% idiopathic Mechanism: ductal obstruction from protein plugs Chronic obstructionchronic and persistent inflammation fibrosis and alternating ductal stricture and dilation Neuronal sheath hypertrophy and peri-neural inflamchronic pain DM in 20-30% in 10-15 yrs due to loss of endocrine function

  27. S&S Episodic abd pain in 85-90% Severe pain, lasts hours to days Episodes subside in 6-10 years, after acinar cells destroyed Steatorrhea when lipase and protease are <10% of normal Greasy stools, oil droplet leakage Sort of like eating a bag of Olestra WOW! Chips Weight loss

  28. Dx Chronic Pancreatitis Difficult to dx Amylase/lipase are normal early Typical alcohol hx helps X-ray show calcification in 30%- but not until late in disease process Without typical hx, must r/o malignancy with abd CT If nl, ERCP, endoscopic US, secretin pancreatic function testing

  29. Tx Similar to acute pancreatitis Acutely: NPO, fluids, opioids Long term: EtOH cessation, low-fat diet to  pancreatic enzyme secretion Often these don’t help; may need  opioids, with real concern for addiction Surgery (pancreatic resection) for pts abstinent from EtOH who can manage DM

  30. Drugs Tx steatorrhea with pancreatic supplements 30,000 units of lipase given before, during, after meals  acid-stimulated release of secretin H2 blocker (ranitidine150 mg BID PPI (omeprazole 20-60 mg qday)‏ Sodium bicarb 650 mg ac and pc

  31. Gallbladder

  32. Anatomy 101 Anatomy of Biliary Tree R & L hepatic ducts from liver form Common Hepatic Duct Joins Cystic Duct from GB to form Common Bile Duct Pancreatic Duct joins at Ampulla of Vater, has Sphincter of Oddi Enters duodenum at Major Duodenal Papilla

  33. Biliary Disease Cholestasis – impairment of bile formation or transport from metabolic, autoimmune, infectious, genetic, or toxic abnormalities Most biliary disease is caused by gallstones Found in 20% ♀ and 8% ♂ > 40 y.o. Biliary sludge: thick mucoid stuff contains phospholipids, cholesterol and Ca++ crystals Precursor to gallstones

  34. Gallstone Formation Gallstones mostly cholesterol, bilirubin, and Ca++ salts, plus proteins and other materials 80% of stones are cholesterol stones, 20% are pigment stones Cholesterol stones form when bile supersaturated with cholesterol Multilaminar vesicles of phospholipid and cholesterol form nucleus of stone Insoluble cholesterol crystals laminate onto surface and grow within mucin gel Polar bile proteins then fuse crystals into stones

  35. Pigment Stones Ca++ salts of bilirubin Often in polymers with mucin glycoproteins, some cholesterol About 15% of stones can be seen on X-ray, and 2/3 of these are pigment stones (more calcified)‏ Why these form is not well understood, but some links to infection and other processes

  36. Etiol/Epidemiology Cholesterol stone formation factors are proportions of cholesterol, phospholipid, and bile acids in gall bladder Stones form when cholesterol output increased or bile acid secretion decreased or combination of both Process enhanced by estrogen and cholesterol Female, OCP, multiparous, over forty Obesity; rapid weight loss and fasting Serum cholesterol not a predictor

  37. Cholelithiasis Presence of one or more calculi in gallbladder In US, 20% of people >65 have stones Most disorders of biliary tract are caused by stones 80% asymptomatic Sx and disease when stones cause obstruction

  38. Cholelithiasis Consequences: Cholecystitis Bile tract obstruction/biliary colic Infection (cholangitis)‏ Gallstone pancreatitis

  39. Biliary colic Caused by transient cystic duct obstruction RUQ pain, poorly localized Sudden onset, peaks in 15-30 min, steady for 1-6h, dissipates over 30-60 min, leaving dull ache If lasts >6h, suspect pancreatitis or cholecystitis, not colic

  40. Biliary Colic Intensify 30-60 minutes after eating (why?), resolves in hours Eructation, N/V, dyspepsia, flatulence, reflux Mild transient elev serum bili >5 Broad, scary DDx, incl PUD, pancreatitis, cardiac syndromes, SBO, AAA, pleurisy, hepatitis, gastroenteritis, PTX

  41. Biliary colic Pain- severe N/V, no F/C Labs normal Feels FINE between episodes Tests: Abd US 95% specific for stones CT, MRI Endoscopic US if other tests equivocal

  42. CholelithiasisPrognosis Asymptomatic stones get symptomatic at average rate of 2% per year Diabetics prone to complications, so recommend cholecystectomy even in absence of sx Symptomatic: Colic resolves spontaneously but recurs in 20-40% of pts per year Complications: cholecystitis, choledocholithiasis, cholangitis, gallstone pancreatitis

  43. Cholelithiasis Treatment Elective cholecystectomy Open Laparoscopic Converts to open in 5% due to difficulty in identifying anatomy or complications Non surgical High risk (age, comorbidities)‏ Stones can be dissolved with oral bile salts made from bear bile. $$$, lots of SEs, lifetime tx

  44. Cholecystitis Inflammation of gallbladder Usually cystic duct obstruction by stone Stone lodges obstructionbile stasisrelease of inflammatory enzymes Damaged mucosa secretes more fluid into gallbladderdistensioninflammatory mediatorsworse mucosal damage ischemiamore inflammation

  45. Cholecystitis Most commonly a complication of cholelithiasis But 5-10% are acalculous Common for pts to have hx biliary colic RUQ pain and tenderness Develops over hours +/- nausea, vomiting, fever, chills Can lead to bacterial infection, necrosis, perforation

  46. S&S Like biliary colic, but worse and doesn’t resolve Vomiting R subcostal tenderness + Murphy’s sign R sided guarding Low grade fever

  47. IF… … abd pain, fever, rigors, + rebound tenderness- think empyema or perforation …accompanied by jaundice, think common duct obstruction …untreated, 10% will have local perforation, 1% free perfperitonitis

  48. Dx and Tx Dx: US- (incl ultrasonographic Murphy’s sign)‏ If unequivocal, cholescintography (HIDA scan)‏ Check CBC, LFTs, amylase/lipase Expect leukocytosis with L shift, nl LFTs Tx: NPO, IV fluids, opioids, parenteral abx, admit, cholecystectomy in next 24-48h

  49. Cholecystitis Complications Emphysematous cholecystitis: result of gangrene, gas-producing bacteria (usually Clostridium)‏ Porcelain GB: repeated inflammation causes deposition Ca++ salts in GB wall Fistula Ileus

  50. Choledocholithiasis Common duct stones Most passed from GB, some form in CBD Sx of gallstones plus possible pancreatitis Charcot’s Triad: RUQ pain, jaundice, fever (usually with chills)‏ ERCP - possible stent, sphincterotomy

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