Pancreatitis by hr3kATa1

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									Nutritional Strategies
in Acute Pancreatitis
Kim Feltner
Advisor: Gilbert Boissonneault
University of Kentucky
Overview

    Occurrence and Disease significance
    Pathophysiology
    Signs and Symptoms
    Diagnosis
    Treatment Methods
Pancreatitis
  Incidence ranges from 1-5 cases per 10,000
   people each year
  In 85-90% of patients, will subside in 3-7 days
  Most common causes
    Alcohol, gallstones
  Others
    Hypertriglyceridemia, viral infections (mumps or
     hepatitis), scorpion bites, some drugs such as
     valproic acid, sulfonamides, and thiazide diuretics
     and others
Pathophysiology
  Autodigestion
    Activation of proteolytic enzymes
     trypsinogen, chymotrypsin, and trypsin
     occurs in the pancreas instead of activation
     in the intestinal lumen
    These activated proteolytic enzymes digest
     pancreatic and peripancreatic tissue
    More enzymes become activated causing
     digestion of cellular membranes that cause
     proteolysis, edema, and interstitial
     hemorrhage
Pathophysiology
   Proteases are packaged in precursor form
    and there are also protease inhibitors in the
    acinar cell and in the pancreatic secretions
    preventing autodigestion from occurring
   Death of the acinar cells releases enzymes
    and begins autodigestion
   Death of acinar cells caused by:
      Duct obstruction or reflux of bile or duodenal
       contents into pancreas
      Certain drugs or alcohol
Symptoms

 Abdominal pain
   Steady and boring located epigastrically may
    radiate to back, chest, flanks, or lower
    abdomen
 N/V
Signs


    Low-Grade Fever
    Tachycardia
    Hypotension
    Diminished or absent bowel sounds
    Pain may be relieved by bending forward
     (patient may be curled up)
Signs
  Turner’s Sign
  Discoloration of the
  flanks reflecting tissue
  catabolism of hemoglobin
  May indicate severe
   necrotizing pancreatitis



 From Forbes CD, Jackson WF: Color Atlas and Text of
 Clinical Medicine, 3rd ed. London, Mosby, 2003.
Signs
  Cullen’s sign 
  Faint blue
 discoloration
 around the umbilicus
  Result of
   hemoperitoneum



 http://content.nejm.org.ezproxy.uky.edu/cgi/content/full/340/2/149
Diagnosis

  CT scan may confirm clinical impression
   of pancreatitis
    Sometimes 3 days after dx to identify
     necrotizing pancreatitis
  CT of abdomen may show gallstones
  ERCP if gallstones suspected
    Usually not used after first attack unless
     cholangitis or jaundice
Lab Abnormalities

    ↑ Serum amylase
    ↑ Lipase parallel with amylase
    Hyperglycemia
    Hypocalcemia
    Leukocytosis
    ↑ CRP  suggests pancreatic necrosis
     and also causes ↓ albumin
Severity Assessment
Ranson’s Criteria
  Admission                       Initial 48 hours
    Age > 55yrs                      ↓ Hematocrit > 10%
    WBC > 16,000/mm3                 ↑ BUN > 5 mg/dL
    Blood Glucose >200mg/dL          Serum calcium < 8mg/dL
    Serum LDH > 350                  Arterial Po2 < 60mmHg
     IU/L                             Base deficit > 4 mEq/L
    Serum AST > 250 U/L              Est. fluid
                                       sequestration > 6 L
   0-2 criteria  1% mortality       Development indicates
   3-4 criteria  16%mortality         worsening prognosis
   5-6 criteria  40% mortality
   7-8 criteria 100% mortality
Treatment

  Narcotics for pain
  IV fluids for hydration
  Normally kept NPO to avoid stimulation
   of pancreas until free of pain and N/V
  If pancreatitis does not subside within a
   few days
    Total Parenteral Nutrition (TPN)
    Enteral nutrition
Nutritional Strategies
  NPO
    Nothing by mouth
    Fluids replenished by IV
    Reduces stimulation of the pancreas to prevent
     worsening of the disease state
    Mild cases may begin oral intake within 3-4 days
  Gastric decompression
    Nasogastric tube suction to remove the acidic
     stomach contents and prevent them from reaching
     the jejunum
    Recent studies have really shown no benefit to this
     therapy
Nutritional Strategies
  Total Parenteral Nutrition (TPN)
  Placement of Central Venous Catheter in order
   to provide complete nutrition (internal jugular,
   subclavian)
  May be required if an ileus is present or if
   patient has been NPO for 7-10 days
  Very invasive, should not be used very early in
   pancreatitis
  High risk of catheter related infections and
   sepsis
Nutritional Strategies
  Enteral Nutrition
  Naso-gastric feeding usually preferred
   (inexpensive and easier-no radiology or
   endoscopy)
  Distal to the ligament of treitz produce no
   change in complications, mortality, or length of
   hospital stay
  Enteral feeding has been shown to improve the
   systemic inflammatory response
What Next?
  After free of pain, N/V, bowel sounds return
  Begin with clear liquid diet
     Very few calories (Enlive is a supplement to clear liquids to
      provide more calories)
     Low residue food in liquid form to minimize amt of food to be
      digested in the intestines
  Next step up to full liquid diet
     All liquids added so some protein and fat are available
  Next step up to small meals, low fat, low cholesterol,
   low triglyceride
  May need to provide counseling to patient to avoid
   recurrent attacks
  Avoid alcohol, eat small meals
References
   Arend W.P., Ausiello D., Goldman L., editors. Cecil Textbook of Medicine. 22nd ed.
    Philadelphia: W. B. Saunders; 2004. 779-884.
   Conn's Current Therapy 2004. 56th ed. Philadelphia: W. B. Saunders; 2004. 563-573.
   Fauci B., Hauser K., Jameson L., editors. Principles of Internal Medicine. 15th ed. Vol. 2.
    New York: McGraw Hill; 2001. 2249-2257.
   Green II H.L., Noble J., et al, editors. Textbook of Primary Care Medicine. 3rd ed. St. Louis:
    Mosby; 2001. 1792-1803.
   Heinrich S., Shafer M., Rousson V., Clavien P. Evidence-based treatment of acute
    pancreatitis: a look at established paradigms. Annals of Surgery. 2005 Feb;243(2):154-
    168.
   Marik P.E., Zaloga G.P. Meta-analysis of parenteral nutrition versus enteral nutrition in
    patients with acute pancreatitis. British Medical Journal (2004):1-6.
   Mcphee S. J., Papadakis M.A, Tierney, Jr L.M., editors. Current Medical Diagnosis and
    Treatment. Los Altos: California: Lange Medical Publications; 2005. 671-676.
   Radenkovic D., Johnson C. Nutritional support in acute pancreatitis. Nutritonal in Clinical
    Care. 2004; 7(3):98-103.
   Raimondo M., Scolapio J.S. What route to feed patients with severe acute pancreatitis:
    vein, jejunum, or stomach? The American Journal of Gastroenterology. 2005
    Feb;100(2):440
   Retally C.A., Skarda S., Garza M.A, Schenker S. The usefulness of laboratory tests in the
    early assessment of the severity of acute pancreatitis. Critical Reviews in Clinical
    Laboratory Science. 2003; 40(2):117-149
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