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Transcript
Pancreatic and Biliary Disease: An Overview Tory Davis PA-C Table of Contents Pancreatic disease – Acute pancreatitis – Chronic pancreatitis Gallbladder disease – Cholelithiasis – Cholecystitis 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, vomitinginflammation confined to gland, 5% mortality) to severe (really bad, maybe dead: pancreatic necrosis, systemic inflammatory process, shock, multi-organ failure- up to 50% mortality) 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 Then what? Cytokines and enzymes in peritoneum cause chemical burns, fluid thirdspacing In systemic circ systemic inflammatory response capillary permeability and vascular tone – acute respiratory distress, renal failure Who’s responsible for this mess? EtOH- 100 g/d x 3-5 yrs (lots)pancreatic enzyme proteins to precipitate in small ductulesobstructionpremature activation of enzymes Biliary/structural- gallstone in Sphincter of Oddi ductal pressures Etiology 80% caused by alcohol or biliary tract disease/structural disorders – Stones – ERCP (dx imaging study) – Trauma – Ischemia – Vasculitis – Pancreas divisum – predisposes for pancreatitis 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 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) 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 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 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 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 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 Ddx Perforated ulcer (gastric, duodenal) Mesenteric infarction Strangulating intestinal obstruction Dissecting aneurysm Biliary colic Appendicitis Inferior wall MI Splenic hematoma Abd muscle hematoma 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 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 Ranson’s Criteria Mortality proportional to # of criteria Download to your PDA for IM rotations… Number of Criteria 0-2 3-4 5-6 7-8 Mortality 1% 16% 40% 100% 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 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 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) 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 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 Other complications Intravascular volume depletion, shock Prerenal azotemia – May require peritoneal or hemodialysis ARDS- acute respiratory distress syndrome Pancreatic abscess- needs drainage GI bleed Chronic Pancreatitis Persistent inflammation of pancreas permanent structural damage decrease in endocrine and exocrine functions Chronic Pancreatitis In US, 70-80% from alcohol, 15-25% idiopathic Mechanism: ductal obstruction from protein plugs – Chronic obstructionchronic and persistent inflammation fibrosis and alternating ductal stricture and dilation – Neuronal sheath hypertrophy and peri-neural inflamchronic pain – DM in 20-30% in 10-15 yrs due to loss of endocrine function 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 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 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 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 Gallbladder 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 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 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 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 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 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 Cholelithiasis Consequences: – Cholecystitis – Bile tract obstruction/biliary colic – Infection (cholangitis) – Gallstone pancreatitis 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 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 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 Cholelithiasis Prognosis 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 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 Cholecystitis Inflammation of gallbladder Usually cystic duct obstruction by stone Stone lodges obstructionbile stasisrelease of inflammatory enzymes Damaged mucosa secretes more fluid into gallbladderdistension inflammatory mediatorsworse mucosal damage ischemiamore inflammation 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 S&S Like biliary colic, but worse and doesn’t resolve Vomiting R subcostal tenderness + Murphy’s sign R sided guarding Low grade fever 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 perfperitonitis 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 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 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 Cholangitis Painful inflammation of biliary tree If infection occurs, then can be suppurative Ascending Cholangitis: rises to infect liver May form obstructing empyema, abscess, gangrene, perforation fulminant liver failure, peritonitis, sepsis (death, too) Suppurative cholangitis is life threatening SCU admission, abx, supportive care, surgical consult Primary Biliary Cirrhosis Inflammation & necrosis of cholangiocytes in small and mid-size bile ducts Immunologic process Cholestatic process results in liver dz Signs/Sx of biliary obstruction – Pruritis, RUQ pain, indigestion, xanthomas and xanthelasmas, eventual cirrhosis and liver failure Mostly ♀ > 40 with co-morbid auto-immune disorders Biliary Dyskinesia Can have all sx of cholecystitis, but no stones, no sludge Usually dysfunction at Sphincter of Oddi
