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Title: Journal reading Evaluation of Factors That Have Reduced Mortality From Acute Pancreatitis Over the P


1
Journal reading Evaluation of Factors That Have
Reduced Mortality From Acute Pancreatitis Over
the Past 20 years
  • Presenter ??? Instructor ???VS

2
Authors
  • Bank, Simmy M.D., F.R.C.P., F.A.C.G. Singh,
    Pankaj M.D. Pooran, Nakechand M.D. Stark,
    Bernard M.D.
  • From the Division of Gastroenterology, Albert
    Einstein College of MedicineLong Island Jewish
    Hospital, New York, New York.
  • Journal of Clinical Gastroenterology, Volume
    35(1), July 2002, pp 50-60

3
Background
  • Reduced mortality rate of acute pancreatitis in
    recent 20 years

4
Goals
  • Investigate the reasons for the reduction in
    mortality.

5
Study
  • 20-year prospective assessment of mortality as it
    relates to the severity of the disease,
    compications and current therapy.
  • Divided into four 4-year periods

6
Mortality changes
  • Over all 10 to 15 ? 4 to 7
  • Severe 15 to 90 ? 20 to 50
  • Scottish study 67 of the deaths occurred within
    the first week
  • Most common causes of deathinfective necrosis,
    GI bleeding, abscess or cyst formation

7
FACTORS THAT HAVE REDUCED MORTALITY FROM ACUTE
PANCREATITIS OVER THE PAST 20 YEARS
  • 1. Recognition and use of the severity signs to
    direct the place, timing, and type of therapy
  • 2. Improvement in intensive care unit (ICU) care
    of patients with respiratory insufficiency
  • 3. Computed tomography (CT) scan
  • 4. Recognition and treatment of the etiology
  • 5. Newer antibiotics
  • 6. Treatment of complications
  • 7. Infective necrosis and fine-needle aspiration
    (FNA)
  • 8. Treatment of cysts
  • 9. Gastrointestinal bleeding
  • 10. Ascites, pleural effusion, pericarditis

8
RECOGNIZING AND USING SIGNS OF SEVERITY
  • Ransons signs
  • Biochemically oriented
  • Severity assessed at 48 hours
  • Sensitivity and specificity 80 to 85
  • Require age adjustment for gallstones, hepatic
    dysfunction, ascites and renal impairment

9
Ranson criteria
10
Imries Glasgow classification
Interpretation minimum score 0 maximum score
8 If the score gt3 severe pancreatitis
likely. If the score lt 3 severe pancreatitis is
unlikely.
11
RECOGNIZING AND USING SIGNS OF SEVERITY
  • Banks clinical criteria
  • Clinically oriented.
  • Sign or organ dysfunction out sie the abdomen

12
Banks clinical criteria
13
RECOGNIZING AND USING SIGNS OF SEVERITY
  • Balthazars score
  • On contrast enhanced CT
  • Poor correlation with Apache II score

14
Balthazars score
15
RECOGNIZING AND USING SIGNS OF SEVERITY
  • Others
  • CRP
  • SIRS
  • IL-6
  • IL-8
  • Pydidinium split product (5 hrs)
  • Trypsinogen-activating peptite
  • hemoconcentration

16
RECOGNIZING AND USING SIGNS OF SEVERITY
  • Improved ICU care or the use of severity signs
    contributed significantly to a reduction in
    mortality associated with acute pancreatitis?

17
FACTORS THAT HAVE REDUCED MORTALITY FROM ACUTE
PANCREATITIS OVER THE PAST 20 YEARS
  • 1. Recognition and use of the severity signs to
    direct the place, timing, and type of therapy
  • 2. Improvement in ICU care of patients with
    respiratory insufficiency
  • 3. CT scan
  • 4. Recognition and treatment of the etiology
  • 5. Newer antibiotics
  • 6. Treatment of complications
  • 7. Infective necrosis and FNA
  • 8. Treatment of cysts
  • 9. Gastrointestinal bleeding
  • 10. Ascites, pleural effusion, pericarditis

18
CT
  • Early CT ( within 48 72 hours) has more or less
    the same specificity and sensitivity as Ranson or
    Bank
  • Contrast aggravate pancreatitis and sequelae

19
FACTORS THAT HAVE REDUCED MORTALITY FROM ACUTE
PANCREATITIS OVER THE PAST 20 YEARS
  • 1. Recognition and use of the severity signs to
    direct the place, timing, and type of therapy
  • 2. Improvement in ICU care of patients with
    respiratory insufficiency
  • 3. CT scan
  • 4. Recognition and treatment of the etiology
  • 5. Newer antibiotics
  • 6. Treatment of complications
  • 7. Infective necrosis and FNA
  • 8. Treatment of cysts
  • 9. Gastrointestinal bleeding
  • 10. Ascites, pleural effusion, pericarditis

20
Assessment of etiology
  • alcohol
  • Gallstones
  • ERCP
  • Idiopathy
  • Hyperlipidemia
  • Post-operation
  • Afferent loop obstruction
  • Duodenal Crohns disease, parathion poisoning
  • Hypercalcemia

21
THE ROLE OF EARLY ERCP IN ACUTE PANCREATITIS
  • Urgent ERCP
  • Cholangitis associated with pancreatitis
  • Severity signs change from mild to severe
  • Elective ERCP
  • Indirect evidence of stone exists
  • Clearly indicated in
  • Stone identified at the ampulla

22
MEDICAL MANAGEMENT OF ACUTE PANCREATITIS
  • Antibiotics
  • Nutrition support
  • Newer drugs

23
Antibiotics
  • Start antibiotics with severe attacks, esp. if
    the CT shows 30 necrosis.
  • Antibiotics penetrating pancreatic tissue and to
    sterilize the gut to prevent bacterial
    translocation
  • Imipenem
  • Ciprofloxacin
  • metronidazole,
  • Bacitracin
  • Reduction mortality among patients with septic
    complications receiving prophylactic antibiotics.

24
Antibiotics
  • Alcohol increases intestinal macrophage
    apoptosis, macrophage-activating factors
  • Use, timing, type, /- ampho-B, diflucan?
  • All acute necrotizing patients should be given
    prophylaxis with an antibiotic.

25
Nutritional Support
  • IV hydration with dextran and NG suction during
    an attack of acute pancreatitis.
  • Prolonged attack (3 5 days) ?
  • TPN
  • increase the incidence of infection
  • Enteral feeding
  • maintains the integrity of the mucosa
  • Preventing bacterial translocation to the
    necrotic pancreas

26
Nutritional Support
  • Jejunal feeding
  • route of choice
  • NG elemental diets feeding
  • May do the same job

27
Newer Drugs
  • diets, bile injection, cholecystokinin
    stimulation, cerulin stimulation, and ischemic
    shock
  • proglumide, octreotide, gabexate, IL-10 and newer
    cytokines, steroids, aprotonin
  • IL-10 vasodilators, dextran, and possibly
    antioxidants

28
Complications
  • Infected and Sterile Necrosis
  • Cyst Formation
  • Gastrointestinal Hemorrhage

29
Infected and Sterile Necrosis
  • FNA timing ?
  • Surgical or nonsurgical management of sterile
    necrosis
  • Early recognition of infected necrosis

30
Cyst Formation
  • Formation result from
  • liquefaction of an intra-or extrapancreatic fluid
    collection
  • direct disruption of a duct, with a high-enzyme
    pancreatic juice collection, which may
    communicate with the ductal system
  • Important factors
  • early recognition,
  • careful radiologic follow-up evaluation
  • timely drainage of cysts

31
Gastrointestinal Hemorrhage
  • Mechanisms
  • splenic vein compression
  • bleeding from short gastric vessels
  • erosions of an abscess or cyst into the gastric
    duodenal, colonic, or retroperitoneal vessels
  • bleeding from a preformed cyst from erosion of
    vessels in the cyst wall
  • aneurysm formation of major vessels (e.g.,
    splenic, pancreatic, or duodenal)
  • pressure ulcers in the stomach
  • portal hypertension resulting from cyst
    compression of the portal vein

32
CONCLUSION
  • importance the factors most responsible for the
    improved prognosis
  • 1. Improved technology for the diagnosis and
    treatment of complications.
  • 2. Advances in antibiotic therapy, with 3rd- and
    4th-generation antibiotics and the recognition of
    fungal overgrowth and its therapy
  • 3. Advances in ICU care
  • 4. Urgent ERCP for associated cholangitis or
    increasing severity scores esp. if CBD stone can
    be documented by sonography and laboratory tests.
  • 5. Tailored surgery for sterile necrosis
  • 6. Improved nutritional support by the enteral
    route
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