Pancreatic_ Hepatic and Biliary Disease_ An Overview - UNEPA.ppt by malj


									  Pancreatic and
Biliary Disease: An

    Tory Davis PA-C
     Table of Contents

   Pancreatic disease
    – Acute pancreatitis
    – Chronic pancreatitis
   Gallbladder disease
    – Cholelithiasis
    – Cholecystitis
      Acute Pancreatitis
   Inflammation of pancreas (+/-adjacent
    – 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)
    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 cytokinesà
  inflammation, edema, tissue necrosis
             Then what?
 Cytokines and enzymes in peritoneum
  cause chemical burns, fluid third-
 In systemic circà systemic
  inflammatory responseà ­apillary
  permeability and ¯ vascular tone
    – acute respiratory distress, renal failure
    Who’s responsible for
         this mess?
   EtOH- 100 g/d x 3-5 yrs
    (lots)àpancreatic enzyme proteins to
    precipitate in small
    activation of enzymes

   Biliary/structural- gallstone in
    Sphincter of Oddià ­   ductal pressures
   80% caused by alcohol or biliary tract
    disease/structural disorders
    – Stones
    – ERCP (dx imaging study)
    – Trauma
    – Ischemia
    – Vasculitis
    – Pancreas divisum – predisposes for
   20% caused by “other”
    – Drugs: ACE-I, sulfa, NSAIDs
    – Infectious: CMV, mumps, Coxsackie B
    – Inherited: CF, other gene mutations
    – Metabolic: hypertrigs, hypercalcemia,
    – 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
   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
   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
    – Grey Turner’s sign: flank ecchymosis
    – Cullen’s sign: umbilical ecchymosis
   Lipase more specific, elevated up to 14
   Amylase elevate early, recedes 3-5 days
          Non-specific to pancreas
   CMP-
    – elevated glucose, $Ca
    – elevated alk phos and bilirubin indicating
   LDH- elevated from tissue necrosis
   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
   Perforated ulcer         Biliary colic
    (gastric, duodenal)      Appendicitis
   Mesenteric
    infarction               Inferior wall MI
   Strangulating            Splenic hematoma
    intestinal               Abd muscle
    obstruction               hematoma
   Dissecting
     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      Mortality
       0-2                     1%
       3-4                     16%
       5-6                     40%
       7-8                     100%
   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,
    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)
 Surgical consult for severe pancreatitis
 ICU admission if oliguric, hypotensive,
  Ranson’s ³ 3, or pancreatic necrosis
  by CT >30%
 Humidified O2 if hypoxic

 Treat heart failure, renal failure,
  hyperglycemia, hypomagnesemia etc
 Abx (imipemem x 1 wk)
   If gallstone pancreatitis:
   80% will pass stone spontaneously within
   If not…ERCP w/ sphincterotomy and stone

   If they DO pass the stone spontaneously,
    may elect lap cholecystectomy later
             Oh and..
 After 5-7d, necrotic tissue can become
 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
 Pancreatic abscess- needs drainage

 GI bleed
   Persistent inflammation of pancreasà
    permanent structural damage à
    decrease in endocrine and exocrine
    Chronic Pancreatitis
 In US, 70-80% from alcohol, 15-25%
 Mechanism: ductal obstruction from
  protein plugs
    – Chronic obstructionàchronic and
      persistent inflammationà fibrosis and
      alternating ductal stricture and dilation
    – Neuronal sheath hypertrophy and          peri
      -neural inflamàchronic pain
    – DM in 20-30% in 10-15 yrs due to loss of
      endocrine function
   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

 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
 Surgery (pancreatic resection) for pts
  abstinent from EtOH who can manage
   Tx steatorrhea with pancreatic
    – 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
           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
          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
   Why these form is not well understood, but
    some links to infection and other processes
   Cholesterol stone formation factors are proportions
    of cholesterol, phospholipid, and bile acids in gall
   Stones form when cholesterol output increased or
    bile acid secretion decreased or combination of
   Process enhanced by estrogen and cholesterol
    – Female, OCP, multiparous, over forty
    – Obesity; rapid weight loss and fasting
    – Serum cholesterol not a predictor
 Presence of one or more calculi in
 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

   Consequences:
    – Cholecystitis
    – Bile tract obstruction/biliary colic
    – Infection (cholangitis)
    – Gallstone pancreatitis
             Biliary colic
 Caused by transient cystic duct
 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,
 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
   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
   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
   Inflammation of gallbladder
   Usually cystic duct obstruction by stone
   Stone lodgesà obstructionàbile
    stasisàrelease of inflammatory enzymes
   Damaged mucosa secretes more fluid into
    gallbladderàdistensionà ­   inflammatory
    mediatorsàworse mucosal damageà
    ischemiaàmore inflammation
   Most commonly a complication of
   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,
 Like biliary colic, but worse and
  doesn’t resolve
 Vomiting

 R subcostal tenderness

 + Murphy’s sign

 R sided guarding

 Low grade fever
 …­ abd pain, fever, rigors, + rebound
  tenderness- think empyema or
 …accompanied by jaundice, think
  common duct obstruction
 …untreated, 10% will have local
  perforation, 1% free perfàperitonitis
                Dx and Tx
   Dx: US- (incl ultrasonographic Murphy’s
   If unequivocal, cholescintography (HIDA
   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
 Emphysematous cholecystitis: result of
  gangrene, gas-producing bacteria
  (usually Clostridium)
 Porcelain GB: repeated inflammation
  causes deposition Ca++ salts in GB
 Fistula

 Ileus
 Common duct stones
 Most passed from GB, some form in
 Sx of gallstones plus possible
 Charcot’s Triad: RUQ pain, jaundice,
  fever (usually with chills)
 ERCP - possible stent, sphincterotomy
   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
   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
     Biliary Dyskinesia
 Can have all sx of cholecystitis, but no
  stones, no sludge
 Usually dysfunction at Sphincter of

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