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pancreatitis (PowerPoint)

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hepatobiliary summary reports from Schwartz' Principles of Surgery 8th ed.

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   Dr. Jocelyn M. Lledo, MD
Dr. Bryan U. Ong Kian Koc, MD
Inflammatory disease of the pancreas assoc.
w/ little or no fibrosis of the gland
Initiated by several factors: gallstones,
alcohol, trauma and infections.
Additional complications: sepsis, shock,
respiratory and renal failure.
Out of 300,000 cases, 10 to 20% of which are
severe, leading to over 3,000 deaths.
Biliary tract disease
   Bile duct stone – most common form of assoc.
    biliary abnormality.
        “ Common channel hypothesis”- blockage below the
         junction of the biliary and pancreatic ducts would cause
         bile to flow into the pancreas, which could then be
         damaged by the detergent action of bile salts.
               Objections:
           1)   Most individuals have a short common bile duct
           2)   Hydrostatic pressure in the biliary tract is lower than in the
   Ductal hypertension resulting from ongoing
    exocrine secretion into an obstructed
    pancreatic duct.
   Colocalization theory of Steer & Saluja -
    zymogens & hyrolases are improperly
    colocalized in a vacuolar structure within the
    pancreatic acinar cell  trypsinogen
    colocalizes w/ cathepsin B  activated
    trypsin  activated digestive enzymes 
    autodigestion of pancreatic acinar cells.
 Consumes for at least 2 years and often
  longer up to 10 years.
 Can be recurrent with continued alcohol
 At least a daily intake between 100 and
  150 g of ethanol  10 to 15% of
  individuals develop pancreatitis & 10-15%
  develop cirrhosis.
   Mechanism of action of ethanol:
        1) “secretion w/ blockage” mechanism - spasm of the
         sphincter of Oddi
         2) Metabolic toxin to pancreatic acinar cells secretory
         increase followed by inhibition  elevation of enzyme
         proteins  aggregate of calcium within protein matrix 
         multiple ductal obstruction  pressure buildup
         3) Ductal permeability  improperly activated enzymes
         leak out of the pancreatic duct into the surrounding
          4) Decreases pancreatic blood flow transiently  focal
         ischemic injury to gland
   1 to 2 % -pancreatic carcinoma
   An episode of pancreatitis – first clinical
    manifestation of a periampullary tumor.
   Blocks secreted juice & its upstream
Iatrogenic Pancreatitis
   Pancreatic biopsy, biliary duct exploration, distal
    gastrectomy, splenectomy
   Bilroth II gastrectomy & jejunostomy
   Cardiopulmonary bypass, cardiac transplantation
   ERCP – 2 to 10 % of patients, due to direct injury
    and/or intraductal hypertension
   Hyperamylasemia, and /or abdominal pain.
   Thiazide diuretics, furosemide, estrogen,
    azathioprine, L- aspqaraginase, 6-
    mercaptopurine, methyldopa, the sulfonamides,
    pentamidine, procainamide, nitrofurantoin,
    dideoxyinosine, valproic acid, and aCh inhibitors.
   Coxsackievirus, Mycoplasma – infecting acinar
   Types I and V hyperlipoproteinemia – abdominal
    pain which is mistaken for acute pancreatitis.
Miscellaneous Causes
 Hypercalcemic states arising from
  hyperparathyroidism  hypersecretion and
  formation of calcified stones intraductally.
 Ascaris and Clonorchis sinensis

 Cholangiocarcinoma

 PRSSI gene

 Pancreatitis divisum
Initial events leading to the onset of
   enteropeptidases acts on zymogens to produce
   Pancreas protects itself by segregating the
    zymogens granule by enclosing them within
    membrane- bound organelles.
   Several injuries attained by the pancreas.
      3 reasons for this theory:
     1) Pancreas is digestible by the activated enyzmes in the
     2) Activated digestive enzyme found within the pancreas
     3) Histology of pancreatitis = suggestive of coagulative
Factors determining the severity of
   Balance between the proinflammatory and
    antiinflammatory factors
        Antiinflammatory factors: anti-TNF-  Ab, IL-1
         receptor antagonist, anti-ICAM1 and anti-CD3
         Abs, IL 10, recombinant PAF acetylhydrolase,
         calcineurin antagonist FK506
   Inhibition of intrapancreatic trypsinogen &
    NF- activation
 Severe pain following generally a
  substantial meal
 Pain is epigastric which radiates to the
  back  relieved by leaning forward
 Vomiting does not relieve the pain
Physical Exam:
   Tachycardia, tachypnea, hypotension, and
   Voluntary and involuntary guarding over epigastric
   Bowel sounds are decreased or absent
   No palpable masses
   Abdomen may be distended w/ intraperitoneal
   Pleural effusion, left
   Necrotizing pancreatitis: Cullen’s sign, Grey
    Turner’s sign
 Hemoconcentration  elevated Hct
 Severe fluid loss  prerenal azotemia

 Hyperglycemia

 Hypoalbuminemia

 Hypocalcemia
Serum Markers
   Serum amylase concentration increases almost
    immediately with the onset of disease and peaks
    within several hours.
        Elevated for 3 to 5 days
        May be measured in the urine elevated after serum
         returns to normal
        Using -amylase makes the diagnosis more specific (88
         to 93%)
   Other markers= 77- 96% specificity (highest for
   Best way to confirm the presence of gallstones in
    suspected biliary pancreatitis
   Extrahepatic ductal dilatations, pancreatic edema,
    swelling & peripancreatic fluid collections
   20% unsatisfactory bec. of bowel gas
CT scanning – more commonly used to
diagnose & distinguish nonnecrotic from more
severe necrotizing or infected pancreatitis
Assessment of Severity
   Early Prognostic Signs: Ranson’s Criteria
        < 2: mortality 0
        3-5: 10-20%
        > 7: > 50%
        Best used w/in initial 48 hrs of hospitalization
   APACHE-II (Acute Physiology & Chronic Health
        Vital signs, specific lab parameters, age, chronic health
         status of the pt
        Advantage: immediate assessment of the severity of the
         pancreatitis  8 or more at admission
          Ranson’s Criteria
   For acute pancreatitis not      For acute gallstone
   due to gallstone                pancreatitis
At admission                    At admission
   Age > 55 yo                     Age > 70 yo
   WBC > 16000/mm3                 WBC > 18000/mm3
   Bld glucose >200 mg/dl          Bld glucose >230 mg/dl
   Serum LDH >350 IU/L             Serum LDH >400 IU/L
   Serum AST >250 U/dl             Serum AST >250 U/dl
During the initial 48H          During the initial 48H
   Hct fall > 10 pts               Hct fall > 10 pts
   BUN elevation >5 mg/dl          BUN elevation >2 mg/dl
   Serum Ca2+ <8 mg/dl             Serum Ca2+ <8 mg/dl
    Base deficit >4 mEq/L          Base deficit >5 mEq/L
   Estimated fluid loss >6 L       Estimated fluid loss >4 L
   Arterial P02 <60mmHg
Biochemical Markers
 No prognostic value: amylase, lipase
 With prognostic value:
     Acute phase proteins (CRP, 2 macroglobulin,
      PMN-elastase, 1 antitrypsin phospholipase A2)
     IL-6 = distinguish mild from severe forms

     Urinary-trypsinogen activation peptide (TAP)
           Under investigation
           5- to 7-AA peptide released from the N-terminus of
            trypsinogen during its activation
CT Scan with contrast
 Gold standard
 Mild pancreatitis: interstitial edema 
  uniform enhancement of the gland
 Necrotizing pancreatitis: microcirculation
  disrupted  decreased enhancement
 Infected necrosis or pancreatic abscess:
  air bubbles
 Pancreatic Phlegmon
 Pancreatic Abscess
 Pancreatic Pseudocyst
 Pancreatis Ascites
 Involvement of adjacent organs, w/
  hemorrhage, thrombosis, bowel infarction,
  obstructive jaundice, fistula formation or
  mechanical obstruction
 Pulmonary – pneumonia, atelectasis, ARDS,
  pleural effusion
 Cardiovascular – hypotension, hypovolemia,
  sudden death, nonspecific ST-T wave
  changes, pericardial effusion
 Hematologic - hemoconcentration, DIC
 GI hemorrhage, peptic ulcer, erosive
  gastritis, portal vein or splenic vein
  thrombosis w/ varices
 Renal – oliguria, azotemia, renal
  artery/vein thrombosis
 Metabolic – hyperglycemia, hypocalcemia,
  hypertriglyceridemia, encephalopathy,
  sudden blindness (Purtscher’s retinopathy)
 CNS – psychosis, fat emboli, alcohol
  withdrawal syndrome
 Fat necrosis – Intra-abdominal
  saponification, subcutaneous tissue
 Initial tx: conservative intensive care w/
goals of oral food & fluid restriction,
replacement of fluids & electrolytes
parenterally, pain control
Severe acute pancreatitis or when (+)
signs of infection: broad spectrum
antibiotics (i.e. imipenem) & careful
surveillance for complications
Mild Pancreatitis – no systemic complications,
low APACHE-II scores & Ranson’s signs,
sustained clinical improvement, nonnecrotic
on CT scan
   Mostly supportive: physiologic monitoring,
    metabolic support, maintenance of fluid balance
   Rest the pancreas: oral intake restriction
   Nasogastric suction, H2 blockers
   Recent studies: PAF antagonists (PAF
    acetylhydrolase, Lexipafant)
   Pain management w/ buprenorphine,pentazocine,
    procaine Hcl, meperidine (Avoid MORPHINE w/c
    causes spasm of Sphincter of Oddi)
Severe Pancreatitis
 Care in ICU
 Elderly w/ 3 or more Ranson’s – monitored
  carefully despite (-) pain
 May develop ARDS
      Due to systemic release of phospholipase A2
        damage alveolar tissue & pulmo capillaries
      Assisted ventilation w/ PEEP

   Accompanied by CV events (cardiac
    arrhythmia, MI, cardiogenic shock & CHF)
Infections –serious complication; most
common cause of death
 Translocated enteric bacteria, in
  necrotizing pancreatitis
 CT- or UTZ-guided fine-needle aspiration
  for GS/CS of fluid or tissue
 Mortality of >50% unless surgically
  debrided + antibiotics (metronidazole,
  imipenem, 3rd gen cephalosporins)
Sterile Necrosis
 Better prognosis than infected necrosis: 0-
 No systemic cx: supportive care
 Systemic cx + secondary infection: CT-
  guided, fine-needle aspiration
 High APACHE-II & Ranson’s scores +
  systemic toxicity: aggressive debridement,
Pancreatic Abscess
 Occurs 2-6 wks after initial attack
 Tx: external drainage whether surgically or by
  percutaneous catheter-based methods
Nutritional Support
   NPO until clinical condition improves
      3-7 days in mild forms, several wks in complicated
      TPN or by enteral nutrition through a jejunal tube
            Jejunal feeding (still stimulates exocrine secretion) more
             superior than TPN (early atrophy of gut mucosa,
             favoring transmigration of luminal bacteria)
Gallstones – most common cause
When to intervene: controversial
   Urgent intervention (cholecystectomy) w/in 1st 48-72 hrs of
   Briefly delayed intervention (after 72 hrs but during initial
    hospitalization) – give time for pancreas to recover
Otherwise healthy pts w/ obstructive pancreatitis:
cholecystectomy & operative common duct clearance
At high risk: ERCP
Acute biliary pancreatitis w/ persistent obstruction after >
24hrs: emergency endoscopic sphincterotomy & stone

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