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Acute Pancreatitis: Management Update

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Title: Acute Pancreatitis: Management Update


1
Acute Pancreatitis Management Update
  • Jamie S. Barkin, M.D., MACP, MACG, AGAF, FASGE
  • Professor of Medicine
  • University of Miami, Miller School of Medicine
  • Chief, Division of Gastroenterology
  • Mount Sinai Medical Center

2
Overview of Acute Pancreatitis
  • 85 of patients have interstitial pancreatitis
    15 (range 4 47) have necrotizing pancreatitis
  • Among patients with necrotizing pancreatitis, 33
    (range 16-47) have infected necrosis
  • Approximately 10 of patients with interstitial
    pancreatitis experience organ failure, but in the
    majority it is transient
  • Mortality in acute pancreatitis overall, is
    approximately 5 3 in interstitial
    pancreatitis, 17 in necrotizing pancreatitis
  • In necrotizing pancreatitis, mortality 3-fold
    infected vs. sterile necrosis
  • Mortality increases with development of organ
    failure 3 (0-8) and with multi-system organ
    failure 47 (range 28-69)

ACG Practice Guidelines in Acute Pancreatitis Am
J Gastroenterol 20061012379-2400
3
Acute PancreatitisConcepts 2009
  • 1) Volume replacement is the foundation of
    therapy
  • 2) Establish severity
  • Utilize initial laboratory data
  • standardized modalities i.e. Ranson criteria
    require 48 hrs
  • CT abnormalities correlate with severity
  • No need for early CT to establish severity
  • 3) Establish etiology
  • Importance is to prevent recurrence
  • 4) Biliary Pancreatitis
  • Utilize laboratory markers for diagnosis of
    retained CBD
  • ERCP is only for treating patients with
    cholangitis

4
Acute Pancreatitis Concepts 2009
  • 5) Do not use prophylactic antibiotics
  • 6) CT guided aspiration is the diagnostic test
    for pancreatic infection allows directed
    antibiotic therapy

5
Acute PancreatitisConcepts 2009
  • (Cont)
  • 7) Surgical intervention in patients with
    infected pancreatic necrosis but rarely in
    sterile necrosis
  • 8) Early enteral feeding is safe, prevents leaky
    gut and is associated with less complications
    than TPN

6
Definition of Severe Acute Pancreatitis (SAP)
  • SAP is acute pancreatitis with local and/or
    systemic complications
  • Local complications are
  • necrotizing pancreatitis
  • Infected necrosis
  • Pancreatic abscess
  • Peripancreatic fluid collection and pseudocystic
    lesions
  • Systemic complications are
  • Pulmonary and renal failure
  • Shock
  • Cardio-circulatory dysfunctions
  • systemic sepsis
  • coagulation disorder
  • Bradley EL, III. Arch Surg 1993128585-590

7
Acute Pancreatitis Mechanisms of Intra
and-Extrapancreatic Inflammation
  • Mediated by cytokines and other inflammatory
    mediators
  • Activation of inflammatory cells
  • Chemo-attraction of activated inflammatory cells
    to the microcirculation
  • Activation of adhesion molecules allowing the
    binding of inflammatory cells to the endothelium
  • Migration of activated inflammatory cells into
    areas of inflammation
  • ACG Practice Guidelines in Acute Pancreatitis.
  • Am J Gastroenterol 20061012379-2400

8
Acute Pancreatitis
  • Mechanism of organ dysfunction
  • Volume depletion
  • Visceral hypofusion
  • ? Capillary permeability ? bowel permeability
  • ( ? TNF, IL6, angioprotin adipokines)
  • Bacterial translocation
  • SIRS
  • David Whitcomb, M.D.

9
Causes of mortality
Acute Pancreatitis
10
Systemic Inflammatory Response Syndrome (SIRS)
Defined by two or more of the following criteria Pulse gt 90 beats/min Respiratory rate gt 20/min or PCO2 lt32 mmHg Rectal temperature lt36 C or gt38C White blood count lt4,000 or gt12,000/mm3
ACG Practice Guidelines in Acute Pancreatitis Am
J Gastroenterol 20061012379-2400
11
Prognosis in Acute Pancreatitis
Acute Pancreatitis
12
Early Diagnostic Indicators in Acute Pancreatitis
Acute Pancreatitis
Early Indicators of Severity
13
Organ Dysfunction Affects Prognosis in Acute
Pancreatitis
Acute Pancreatitis
Organ Dysfunction Affects Prognosis
A Buter et al., Brit. J. Surgery 2002 89298
14
Obesity Worsens the Prognosis in Acute
Pancreatitis
Autoimmune Pancreatitis
Obesity Worsens Prognosis
60
  • Effect may be greatest with a high waist / hip
    fat ratio
  • Possible Mechanisms
  • Free fatty acids
  • Cytokines (TNFa??IL-6)
  • Reduced diaphragmatic excursion

Severe Pancreatitis
Systemic complications
40
Patients
20
0
lt25
25-29
gt29
Body Mass Index (kg/m2)
J Martinez et al., Pancreas 1999 1915
15
Diagnostic Guideline I Look for Risk Factors of
Severity at Admission
  • Older age (gt55 yrs)
  • Obesity BMI gt 30
  • Organ failure at admission
  • Pleural effusion and/or infiltrates
  • When organ failure is corrected within 48 hours,
    mortality is close to 0
  • When organ failure persists for more than 48 h,
    mortality is 36
  • Level of Evidence III

ACG Practice Guidelines in Acute Pancreatitis Am
J Gastroenterol 20061012379-2400
16
APACHE II score (acute physiology score)
  • Rectal temperature (?C)
  • Mean arterial pressure (mmHg)
  • Heart rate (bpm)
  • Respiratory rate (bpm)
  • Oxygen delivery (mL/min)
  • PO2 mmHg)
  • Arterial pH
  • Serum sodium (mmol/L
  • Serum potassium (mmol/L)
  • Serum creatinine (mg/dL)
  • Hematocrit ()
  • White cell count (103 /mL)
  • History of severe organ insufficiency

ACG Practice Guidelines in Acute Pancreatitis.
Am J Gastroenterol 20061012379-2400
17
Diagnostic Guideline II Determination of
severity by Laboratory Tests at Admission or lt 48
Hours
  • Level of Evidence III
  • Hematocrit 44 at admission and failure of
    admission hematocrit to decrease at 24 h are the
    best predictors of necrotizing pancreatitis
  • Absence of hemoconcentration at admission or
    during the first 24 h is strongly suggestive of a
    benign clinical course
  • C-reactive protein greater than 150 mg/L within
    the first 72 h of disease correlate with the
    presence of necrosis with a sensitivity and
    specificity that are both gt80
  • The peak of c-reactive protein is generally 36
    72 h after admission, therefore this test is
    not helpful at admission in assessing severity
  • ACG Practice Guidelines in Acute Pancreatitis
  • Am J Gastroenterol 20061012379-2400

18
Hematocrit and Severity of Acute Pancreatitis
Acute Pancreatitis
Hematocrit and Severity
Brown J, et al., Pancreas 2000 20367
19
Indications for Computed Tomography (CT) in Acute
Pancreatitis
Acute Pancreatitis
20
Modified CT Severity Index
Ref Mortele K, et al. AJR 20041831261-1265
Prognostic Indicator Points
Pancreatic inflammation Normal Pancreas Intrinsic pancreatic abnormalities with or without inflammatory changes in peripancreatic fat Pancreatic or peripancreatic fluid collection or peripancreatic fat necrosis Pancreatic necrosis None 30 gt30 Extrapancreatic complications (one or more of pleural effusion, ascites, vascular complications, parenchymal complications or gastrointestinal tract involvement 0 2 4 0 2 4 2
Summary Significant correlation with severity
and organ failure
21
Computed Tomography and Magnetic Resonance
Imaging in the Assessment of Acute Pancreatitis
  • Aim To compare the accuracy of magnetic
    resonance imaging with computed tomography in
    assessing acute pancreatitis
  • Method MRI was performed with intravenous
    secretin and contrast medium
  • Results
  • 39 patients were studied
  • Acute pancreatitis was assessed clinically as
    severe in 7 patients
  • Considering the Ranson score, MRI detected severe
    AP with 83 (58-96, 95 CI) sensitivity, 91
    (68-98) specificity vs. 78 (52-93) and 86
    (63-96) for CT
  • Magnetic resonance showed pancreatic duct leakage
    in 3 patients (8)
  • Arvanitakis M, et al. Gastroenterology
    2004126(3)715-23

22
MRI Provides Prognostic Information in Acute
Pancreatitis
Acute Pancreatits
MRI Provides Prognostic Information in Acute
Pancreatitis
CT vs MRI Score
10
8
6
CT-SI
4
2
0
2
4
6
8
10
0
MR-SI
Arvanitakis, Gastro 2004, 126
23
Diagnostic Guideline IIIDetermination of
Severity During Hospitalization
  • Contrast-Enhanced CT Scan
  • Not on admission if diagnosis is determined -
  • A few days after admission to distinguish
    interstitial from necrotizing pancreatitis when
    there is clinical evidence of increased severity.
    Level of Evidence III
  • To guide aspiration in patients with fluid
    collection to determine if infected
  • ACG Practice Guidelines in Acute Pancreatitis
  • Am J Gastroenterol 20061012379-2400

24
Etiologies of acute pancreatitis
Acute Pancreatitis
Etiologies
25
Acute Idiopathic Pancreatitis does it really
exist or is it a myth?
  • Background
  • Gallstones and alcohol abuse are the most
    frequent causes (75 of patients) of acute
    pancreatitis
  • Consider hyperlipidemia, hypercalcemia and drugs
  • In 10 to 40, no cause is identified
  • Identifying a cause in these patients is
    important, since the recurrence rate is high

Van Brummelen SE, et al. Scand J Gastroenterol
(Suppl) 2003(239)117-22
26
Microlithiasis is the Most Common Cause Acute
Idiopathic Pancreatitis
  • Results
  • Microlithiasis or biliary sludge is an important
    cause of acute idiopathic pancreatitis in up to
    80 of patients
  • Microlithiasis can be detected by
    trans-abdominal/endoscopic ultrasonography or
    polarizing light microscopy of bile
  • Acute pancreatitis can be prevented by performing
    cholecystectomy and opening the sphincter of Oddi

Adapted from Van Brummelen SE, et al. Scand J
Gastroenterol (Suppl) 2003(239)117-22
27
Microlithiasis Effect of Treatment
Microlithiasis Effect of Treatment
E Ros, Gastroenterology 1991 1011701 SP Lee, N
Engl J Med 1992, 326589
28
Etiologies of acute pancreatitis expanded
Acute Pancreatitis
Etiologies
29
Drug-Induced Pancreatitis
  • 1.4 to 2.0 of patients
  • Mechanism hypersensitivity - early vs. toxic
    metabolite (usually lt12 weeks)

30
Drug induced pancreatitis sorted by incidence
Acute Pancreatitis
31
Drug Induced Acute Pancreatitis 2009
  • Isoniazid
  • Pegylated interferon alfa-2b
  • Clarithromycin
  • Metronidazole
  • Trimethoprim - sulfamethoxazole
  • Atorvastatin, Rosuvastatin, Simvastatin
  • Estrogen/Tamoxifen
  • Propofol
  • Jawaid Q, et al. Dig Dis Sci 200247(3)614-17
  • Tosun E, et al. Acta Cardiol 200459(5)571-572
  • Chow KM, et al. Van Zuiden Communications
    200462(1)
  • Cecchi E, et al. Emergency Medicine Australasia
    200416473-475
  • Schouwenberg BJJW, Deinum J. van Zuiden
    Communication 200361(7)
  • Singh S, et al. JOP J Pancreas 20045(6)502-504
  • Perego E, et al. JOP J Pancreas 20045(5)353-356
  • Nigwekar SU, Casey KJ. JOP J Pancreas
    20045(6)516-519
  • Neth J med 200563275

32
Infections and pancreatitis
Acute Pancreatitis
33
Infectious Causes of Acute Pancreatitis2003-2009
  • Measles
  • Herpes Simplex
  • Hepatitis
  • A
  • B, C
  • E
  • HIV
  • Takebayashi K, et al. Trop Gastroenterol 2003
  • Khanna S, Viji JC. Trop Gastroenterol
    200324(1)25-6
  • Makharia GK, et al Trop Gastroenterol
    200324(4)200-01
  • Tyner R, Turett G. South Med J 200497(4)393-94
  • Shintaku M, et al. Arch Pathol Lab Med
    2003127231-234

34
Other Causes of Acute Pancreatitis
  • Inflammatory bowel disease
  • Crohns (not 5 ASA) 4-fold
  • Ulcerative colitis 1.5 fold
  • Ischemia
  • systemic lupus
  • sickle cell crisis
  • Preeclampsia-eclampsia
  • Toxins carbofuran insecticides
  • Organophosphates
  • Fan HC, et al. J Microbial Immunol Infect
    200336(3)212-4
  • Ahmed S,et al. Am J Hematol 2003 73(3)190-3
  • Parmar MS. JOP 20045(2)101-4
  • Rizos E, et al. JOP 20045(1)44-7
  • Munk AM J Gastro 2004

35
Acute Pancreatitis
Hypertriglyceridemia
36
Tumors as Causes of Acute Pancreatitis
  • Primary
  • Pancreatic adenocarcinoma
  • IDPMT
  • Ampullary tumors
  • Lymphoma
  • Adult T-cell leukemia/lymphoma
  • Metastases
  • Lung
  • Salva R, et al. Ann Surg 2004239(5)678-85
  • Adv Thr 200522225
  • Mori A, 2003 DDS

37
Acute Biliary Pancreatitis
  • Goals are to identify
  • patients whose stones have not passed
  • patients with complications of stones
    cholangitis
  • ERCP is done only if there is biliary obstruction
    with cholangitis

38
Biliary Pancreatitis What happens to CBD stones?
  • Stone or concretion is found in CBD
  • within 48 hours after admission in 62 75
  • After 48 hours post admission CBD stones are
    found in 3 33
  • The natural history of CBD stones is passage

39
The Value of Magnetic Resonance
Cholangio-pancreatography in Predicting CBD
Stones in Patients with Gallstone Disease
  • Results
  • CBD stones were demonstrated in 43 (12) of 366
    patients
  • MRCP had
  • an observed sensitivity of 95
  • specificity of 100
  • positive predictive value of 100 and
  • negative predictive value of 98

Topal B, et al. Br J Surg 20039042-47
40
Treatment Guideline VIIIRole of ERCP and Biliary
Sphincterotomy in Gallstone Pancreatitis
  • Indicated for clearance of bile duct stones in
    patients with severe pancreatitis, in those with
    cholangitis
  • ERCP should be performed primarily in patients
    with high suspicion of bile duct stones when
    therapy is indicated
  • EUS or MRCP can be used to identify common bile
    duct stones
  • Level of Evidence I

ACG Practice Guidelines in Acute Pancreatitis.
Am J Gastroenterol 20061012379-2400
41
Acute Biliary Pancreatitis First 24 to 48 hours
Jaundice with Bilirubin gt 1.35 _at_ 24 hrs
MRCP
ERCP
CBD stones
Neg
Pos
Neg
Pos
Stone removal
Elective surgical cholecystectomy
42
Role of Surgery in Patients with Severe Acute
Pancreatitis
Indication Timing
Biliary pancreatitis Infected necrosis Laparoscopic cholecystectomy during hospitalization or lt 6 weeks after episodes Later gt 10 days unless unstable with infected necrosis
43
Early versus Late Necrosectomy in Severe
Necrotizing Pancreatitis
  • Patients were randomly allocated to two treatment
    arms as follows
  • Group A included early necrosectomy (within 48 to
    72 hours of onset)
  • Group B included late necrosectomy (at least 12
    days after onset)
  • Results
  • Difference in the mortality rate (58 vs. 27)
    was not statistically significant, the odds ratio
    for mortality was much higher in the early
    operation group
  • Early surgery in severe acute pancreatitis is
    only required in cases with proven early
    infection of the pancreatic necrosis (and not
    stable)

Mier J, et al. Am J Surg 199717371-7 Buchler
MW, et al Dig Dis 199210354-62 Mai G, et al
Berlin, Blackwell Science 1999475-85
44
ROLE OF PROPHYLACTIC ANTIBIOTICS IN PATIENTS
WITH SEVERE ACUTE PANCREATITIS
45
The incidence of pancreatic infections increases
with time
Acute Pancreatitis
Adapted from H. Beger et al., Gastroenterology
1986 91433
46
Local and Systemic Infections in Acute
Pancreatitis
  • After week 1, the prognosis . is mainly
    determined by bacterial infection of pancreatic
    and peripancreatic necrosis
  • Mortality increases from 5 - 25 in patients
    with sterile necrosis to 15 - 28 in patients
    with infected necrosis
  • Rau B, et al. J Am Coll Surg 1995181279-288
  • Rau B, et al. World j Surg 199721155-161
  • Isenmann R, et al.Br J Surg 1999861020-1024
  • Wilson PG, et al. J Antimicrob Chemother
    199841(suppl A)51-63
  • Tenner S, et al. Gastroenterology
    1997113899-903
  • Buchler MW, et al. Ann Surg 2000232619-626

47
Preoperative morbidity in patients with infected
and sterile necrosis
Ref Beger, et al. Pancreatology 2005510-19
Bacteriologically positive (45 pts) n Bacteriologically negative (69 pts) n P value
Cardiovascular complications (systemic Pa lt80
mm Hg for gt min 14 31.0
5 7.3 0.001 Pulmonary
insufficiency
(Pa02lt60mm Hg)
18 40.0 10 14.3
0.01 Renal insufficiency (creatinine gt120
?M) 19 42.2 15 21.7
0.02 Sepsis (rectal temperature
gt38.5C leukocytes lt4,000 or gt12,000/mm3
platelets lt150,000/mm3 base excess gt-4
16 35.6 6
8.7 0.001 Gastrointestinal bleeding
8 17.8 4 5.8
0.05 P0.05 by Holms rejective multiple test
procedure
48
Antibiotic Therapy for Prophylaxis Against
Infection of Pancreatic Necrosis in Acute
Pancreatitis
  • Aim to determine the effectiveness and safety of
    prophylactic antibiotic therapy in patients with
    severe acute pancreatitis who have developed
    pancreatic necrosis
  • Results
  • A survival advantage for antibiotic therapy (Odds
    ratio 0.32, p0.02) was demonstrated
  • Pancreatic sepsis showed an advantage for therapy
    (Odds ratio 0.51, p0.04)
  • Extra-pancreatic infection could be evaluated in
    three studies, but showed no significant
    advantage for therapy (Odds ratio 0.47, p0.05)

Cochrane Database Syst Rev 2003(4)CD002941
49
Antibiotic Therapy for Prophylaxis Against
Infection of Pancreatic Necrosis in Acute
Pancreatitis
  • (Cont)
  • Surgery rates were not significantly reduced
    (Odds ratio 0.55, p0.08)
  • Fungal infections showed no strongly increased
    preponderance with therapy (Odds ratio o.83,
    p0.7)
  • Reviewers Conclusion
  • Strong evidence that intravenous antibiotic
    prophylactic therapy for 10 to 14 days decreased
    the risk of super-infection of necrotic tissue
    and mortality in patients with severe acute
    pancreatitis with proven pancreatic necrosis at
    CT
  • Cochrane Database Syst Rev 2003(4)CD002941

50
Prophylactic Antibiotic Treatment in Patients
with Predicted Severe Acute Pancreatitis A
placebo-controlled, double-blind trial
  • Method
  • 114 patients with acute pancreatitis in
    combination with a serum C-reactive protein
    exceeding 150 mg/L and/or necrosis on
    contrast-enhanced CT scan, were enrolled
  • Patients received either intravenous CIP (2 x 400
    mg/day) MET (2 x 500 mg/day) or PLA
  • Study medication was discontinued and switched to
    open antibiotic treatment when infectious
    complications, multiple organ failure sepsis or
    systemic inflammatory response syndrome (SIRS)
    occurred

51
Ciprofloxacin plus metronidazole vs. placebo
in severe acute pancreatitis
Intention-to-treat analysis (114 patients) Ciprofloxacin/ placebo Metronidazole (56 patients) (58 patients) Necrotizing pancreatitis on contrast-enhanced CT scan (76 patients) Ciprofloxacin/ placebo Metronidazole (35 patients) (41 patients)
Mortality Surgical treatment Infected pancreatic necrosis 5 7 17 11 12 9 7 11 24 19 17 14

Isenmann R, et al. Gastroenterology
2004126997-1004
52
Prophylactic Antibiotic Use in Severe Acute
Pancreatitis (SAP) Hemlock, Help or Hype?
  • Concerns
  • A large number of subjects in the treatment arm
    (16 of 58) had their antibiotics switched from
    the study medicines
  • Many individuals in the control group (26 of 56)
    were started on antibiotic therapy during the
    trial period
  • Number of subjects in each of the comparison
    groups was very small and the study was likely
    underpowered to detect a difference in the
    secondary endpoints
  • Brown A. Gastroenterology 20041195-1198

53
Early Antibiotic Treatment for Severe Acute
Necrotizing Pancreatitis
  • Methods
  • Multicenter, prospective, double-blind,
    placebo-controlled randomized study set in 32
    centers
  • Participants
  • One hundred patients with necrotizing
    pancreatitis 50 received meropenem and 50
    received placebo
  • Outcome Measures
  • infection within 42 days
  • Results
  • Pancreatic or peripancreatic infections developed
    in 18 (9/50) of patients in the meropenem group
    compared with 12 (6 /50) in the placebo group

Dellinger EP, et al. Ann Surg 2007245674-683
54
As Good As it GetsThe Study of Prophylactic
Antibiotics in Severe Acute Pancreatitis
  • The studies suffered from a high percentage of
    patients in the placebo group (Isenmann study,
    46 Dellinger study 54) who were treated with
    intravenous antibiotics, although in the
    Dellinger study, these were used late, on
    average, nearly 3 weeks following randomization
  • Placebo group infection rates in both studies
    were only 17 (7/41) in the Isenmann study and
    12 (6/50) in the Dellinger study

Howard TJ. Ann Surg 2007245 (5) 684-85
55
Treatment Guideline IVAntibiotics in Necrotizing
Pancreatitis
  • Level of Evidence III
  • Not recommended at this time in patients with
    necrotizing pancreatitis
  • During the first 7 10 days, patients with
    pancreatic necrosis may appear septic with
    leukocytosis, fever, and/or organ failure
  • Antibiotic therapy is appropriate while an
    evaluation for a source of infection is
    undertaken
  • Once blood and other cultures (including
    CT-guided fine needle aspiration) are found to be
    negative, discontinue antibiotic therapy

ACG Practice Guidelines in Acute Pancreatitis.
Am J Gastroenterol 20061012379-2400
56
Severe Acute Pancreatitis 2009

CT
ESAP
Necrosis gt 30
No Necrosis
?Antibiotics Meropenem for 10-14 days
No antibiotic
57
Management of Pancreatitis Prior to CT-FNA
  • The extent of leukocytosis or temperature does
    not reliably distinguish severe sterile from
    infected necrosis
  • The development of organ failure (or multi-system
    organ failure) and serum markers are not reliable
    indicators of infected necrosis

Buchler MW, et al. Ann Surg 2000232(5)619-26 Mie
r J, et al. Am J Surg 1997173(2)71-5 Rau B, et
al. Br J Surg 199885(2)179-84
58
Severe Acute Pancreatitis Role of CT-guided
Needle Aspiration
  • Infected Necrosis
  • Suspicion
  • Tº gt 100 F
  • elevated WBC
  • unresolved organ failure
  • Recurrence of SIRS or persistence gt 7 days
  • Diagnosis
  • CT guided aspirate for gram stain and Culture and
    sensitivity

59
Percutaneous Aspiration of Pancreatic Fluid
Collection Gram stain and Culture
  • 10 aspirate gram stain negative and culture
    positive
  • No history of antibiotic administered
  • Aspirant gram stain positive with negative
    cultures in 2 of 34 (6) patients
  • Effect of antibiotics on aspirate

Barkin JS, et al. Dig Dis Sci 198126(7)585 Free
ny PC, et al AJR 1998170969-975
60
Value of Percutaneous Aspiration of the Pancreas
(CT-FNA)
  • CT-FNA is safe and accurate in distinguishing
    sterile from infected necrosis
  • CT-FNA results dictate that appropriate
    antibiotics can be initiated based on the results
    of culture and sensitivity and surgical
    debridement
  • Observation and support to overcome organ failure
    should be maintained during the first several
    weeks of acute pancreatitis in patients with
    sterile necrosis based on CT-FNA therapy because
    of the high mortality associated with early
    surgical debridement

Pappas TN. Am J Gastroenterol 20051002371-2374
61
Treatment Guideline VTreatment of Infected
Necrosis
  • CT-guided percutaneous aspiration with Grams
    stain and culture aspirate is recommended when
    infected necrosis is suspected
  • Treatment of choice in infected necrosis is
    surgical debridement
  • Level of Evidence III

ACG Practice Guidelines in Acute Pancreatitis.
Am J Gastroenterol 20061012379-2400
62
Route of Alimentation
Acute Pancreatitis Nutrition
Route of Alimentation
TPN Cost high No pancreas stimulation Increased
infections Electrolyte disturbances Detrimental
to gut integrity
Enteral Cost moderate May stimulate
pancreas Reduced infections Electrolytes
undisturbed May retain gut integrity
63
Acute Pancreatitis
  • Negative effects of TPN
  • Increased gut permeability
  • Increased central catheter-related sepsis
  • Immunosuppressive effects
  • Increased incidence of septic complications
  • Greatly increased costs

64
Total Parenteral Nutrition (TPN) andEnteral
Nutrition (EN)
TPN causes intestinal mucosal atrophy
alterations in the gut associated lymphoid tissue
(GALT) system and a reduction in intestinal
secretory IgA (S-IgA) levels EN prevents
hypermetabolism, maintains immunocompetence and
improves wound healing considered to reduce
septic complications, shorten hospital stay and
reduce the risk of death
Levine GM, et al Gastro 197467975 King BK, et
al. Arch Surg Kudsk KA, et al Ann Surg
1996223629 Mochizuk H, et al Ann Surg
1984200297-310 Alverdy J, et al. Ann Surg
1985202681 Schroeder D, et al JPEN
199115376 Moore FA, et al. J Trauma
198929916.
65
Enteral Feeding
Acute Pancreatitis Nutrition
Enteral Feeding
Safe and well-tolerated Elemental diet causes
less pancreas stimulation Demonstrated
Benefits Reduced infections Fewer metabolic
complications Shorter length of stay Potential
benefits Improved intestinal
permeability Reduced systemic inflammatory
response
66
Enteral vs Parenteral Nutrition
Acute Pancreatitis
Enteral vs Parenteral Nutrition
Favors Favors Study enteral parenteral
Infection
Complications other than infection
Surgical interventions
Mortality
0.1 1 10
Marik PE BMJ 2004 doi10.1136/bmj
67
Meta-analysis of Parenteral Nutrition versus
Enteral Nutrition in Patients with Acute
Pancreatitis
  • Aim To compare the safety and clinical outcomes
    of enteral and parenteral nutrition in patients
    with acute pancreatitis
  • Method
  • 263 participants in the 6 randomized controlled
    studies were analyzed
  • Data Synthesis
  • Enteral nutrition was associated with a
    significantly lower incidence of infections
    (relative risk 0.45 98 confidence interval 0.26
    to 0.78, P0.004), reduced surgical interventions
    to control pancreatitis (0.48, 0.22 to 1.0
    P0.05)
  • A reduced hospital stay (mean reduction 2.9 days,
    1.6 days to 4.3 days, Plt0.001)
  • There were no significant differences in
    mortality (relative risk ).66, 0.32 to 1.37,
    P0.3) or non-infectious complications (0.61,
    0.31 to 1.22, P0.16) between the two groups

Marik, PE, Zaloga GP. BMJ 20043281407-09
68
Nutritional Support and Infection
Acute Pancreatitis
Nutritional Support and Infection
Favors Favors Study enteral TPN
Abou-Assi Gupta Kalfarentzo McClave Olah Windsor
Total (95 CI)
0.01 0.1 1 10 100
Infections
Marik PE, Zaloka GP. BMJ 2004 3281407
69
Treatment Guideline IIINutritional Support
  • Enteral feeding rather than total parenteral
    nutrition is suggested for patients who require
    nutritional support
  • Level of Evidence II
  • In severe necrotizing pancreatitis (especially
    when most or all of the pancreas is necrotic)
    provide potent pancreatic enzymes and then
    evaluate later in the course
  • It is prudent to use a proton pump inhibitor
    because of the likelihood that bicarbonate
    secretion by the pancreas is severely diminished

ACG Practice Guidelines in Acute Pancreatitis Am
J Gastroenterol 20061012379-2400
70
Treatment Guideline ISupportive Care
  • Level of Evidence III
  • 1. Carefully monitored during the first 24 h of
    vital signs, oxygen saturation and fluid balance
    - hypoxemia and inadequate fluid resuscitation
    may be unrecognized for prolonged periods of time
  • Result Early aggressive fluid resuscitation and
    improved delivery of
  • oxygen prevent or minimize
    pancreatic necrosis and improve
  • survival
  • 2. Consequence of hypovolemia is intestinal
    ischemia, which increases
  • intestinal permeability to bacteria and
    endotoxin
  • Result Translocation of bacteria cause
    secondary pancreatic infection
  • and contribute to on-going
    pancreatic injury and also to organ
  • failure

ACG Practice Guidelines in Acute Pancreatitis Am
J Gastroenterol 20061012379-2400
71
Approach to Patients with Severe Acute
Pancreatitis
Support and stabilize
Suggestion of infection after day 5
Organ system failure - Antibiotics ?
CT guided needle aspiration
Positive
Negative
Adjust Antibiotics
Observe and re-aspirate
Stable
Unstable
  • .

Follow
Surgery
72
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