Pancreatitis

Acute Pancreatitis: Management Update

Dr Tapan Shah, MS, DNB, MD;FACS, MACSSURGICAL GASTROENTEROLOGY AND

HEPATOBILIARY SURGEON

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 2006;101:2379-2400

Acute Pancreatitis:Concepts 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

5) Do not use prophylactic antibiotics

6) CT guided aspiration is the diagnostic test for pancreatic infection & allows directed antibiotic therapy



(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

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 1993;128:585-590

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

inflammationACG Practice Guidelines in Acute Pancreatitis.


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.

Causes of mortality

Acute Pancreatitis

DEATH

Early (< one week)• Systemic inflammatory

response syndrome (SIRS)

• Multiorgan failure

Late (> one week)• Multiorgan failure

• Pancreatic infections/sepsis

Systemic Inflammatory Response Syndrome (SIRS)

Defined by two or more of the following criteria:

Pulse > 90 beats/min

Respiratory rate > 20/min or PCO2 <32 mmHg

Rectal temperature <36° C or >38°C

White blood count <4,000 or >12,000/mm3

ACG Practice Guidelines in Acute Pancreatitis Am J Gastroenterol 2006;101:2379-2400

Acute Pancreatitis

Prognosis

• Bedside AssessmentUnderestimates severe disease

• Scoring SystemsRanson, Glasgow, Apache, Rabenek

• Serum MarkersTrypsinogen activation peptide (TAP)C-reactive protein (CRP)Cytokines

• Imaging criteriaFluid collections, necrosis

Prognosis in Acute Pancreatitis

Acute Pancreatitis

Early Indicators of Severity

• Tachycardia, hypotension

• Tachypnea, hypoxemia

• Hemoconcentration

• Oliguria

• Encephalopathy

Early Diagnostic Indicators in Acute Pancreatitis

Acute Pancreatitis

No deteriorating dysfunction

Deteriorating dysfunction

25

100

50

75

0 10 20 30 40 50 60 70 80 900

No organ dysfunction

Organ dysfunction

10 20 30 40 50 60 70 80 90

25

100

50

75

Time (days)

%Survival

rate

Time (days)

Organ Dysfunction Affects Prognosis in Acute Pancreatitis

Organ Dysfunction Affects Prognosis

A Buter et al., Brit. J. Surgery 2002; 89:298

J Martinez et al., Pancreas 1999; 19:15

Effect may be greatest with a high waist / hip fat ratio

Possible Mechanisms

↑ Free fatty acids

↑ Cytokines (TNFα, IL-6)

↓ Reduced diaphragmatic excursionBody Mass Index (kg/m2)

%Patients

0

20

40

60

<25 25-29 >29

Severe Pancreatitis

Systemic complications

Obesity Worsens Prognosis

Autoimmune Pancreatitis

Obesity Worsens the Prognosis in Acute Pancreatitis

Diagnostic Guideline I: Look for Risk Factors of Severity at Admission

Older age (>55 yrs) Obesity – BMI > 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 2006;101:2379-2400

APACHE II score = (acute physiology score)

1. Rectal temperature (°C)2. Mean arterial pressure (mmHg)3. Heart rate (bpm)4. Respiratory rate (bpm)5. Oxygen delivery (mL/min)6. PO2 mmHg)7. Arterial pH8. Serum sodium (mmol/L9. Serum potassium (mmol/L)10. Serum creatinine (mg/dL)11. Hematocrit (%)12. White cell count (103 /mL)13. History of severe organ insufficiency

ACG Practice Guidelines in Acute Pancreatitis. Am J Gastroenterol 2006;101:2379-2400

Diagnostic Guideline II: Determination of severity by Laboratory Tests at Admission or < 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 >80%

–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 PancreatitisAm J Gastroenterol 2006;101:2379-2400

Hematocrit and Severity

Criteria Incidence of Necrosis

Admission hematocrit >44% 50%OR fails to fall over

first 24 hours

Neither present 4%

Acute Pancreatitis

Brown J, et al., Pancreas 2000; 20:367

Hematocrit and Severity of Acute Pancreatitis

Acute Pancreatitis

Computed Tomography: Indications

•Diagnosis

•Prognosis

•Detect complications

Indications for Computed Tomography (CT) in Acute Pancreatitis

Modified CT Severity Index

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% >30%

Extrapancreatic complications (one or more of pleural effusion, ascites, vascular complications, parenchymal complications or gastrointestinal tract involvement

02

4

0242

Summary: Significant correlation with severity and organ failure

Ref: Mortele K, et al. AJR 2004;183:1261-1265

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 2004;126(3):715-23

MRI Provides Prognostic Information in Acute Pancreatitis

CT vs MRI Score

MR-SI

CT-SI

2 4 6 8 10

8

10

6

4

2

Arvanitakis, Gastro 2004, 126

00

MRI Provides Prognostic Information in Acute Pancreatitis

Acute Pancreatits

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


Acute Pancreatitis

Etiologies of acute pancreatitisEtiologies

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

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

Microlithiasis: Effect of Treatment

E Ros, Gastroenterology 1991; 101:1701SP Lee, N Engl J Med 1992, 326:589

%with

recurrent pancreatitis

0

20

40

60

80

100

Untreated Treated

Ros 91Lee 92

Microlithiasis: Effect of Treatment

Acute PancreatitisEtiologies of acute pancreatitis expandedEtiologies

Drug-Induced Pancreatitis

1.4% to 2.0% of patients

Mechanism – hypersensitivity - early vs. toxic metabolite (usually <12 weeks)

Acute PancreatitisDrug induced pancreatitis sorted by incidence

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 2002;47(3):614-17

Tosun E, et al. Acta Cardiol 2004;59(5):571-572

Chow KM, et al. Van Zuiden Communications 2004;62(1)

Cecchi E, et al. Emergency Medicine Australasia 2004;16:473-475

Schouwenberg BJJW, Deinum J. van Zuiden Communication 2003;61(7)

Singh S, et al. JOP J Pancreas 2004;5(6):502-504

Perego E, et al. JOP J Pancreas 2004;5(5):353-356

Nigwekar SU, Casey KJ. JOP J Pancreas 2004;5(6):516-519

Neth J med 2005;63:275

Acute Pancreatitis

Infections and pancreatitis

Infectious Causes of Acute Pancreatitis:2003-2009

Measles Herpes Simplex Hepatitis

A B, C E

HIV

Takebayashi K, et al. Trop Gastroenterol 2003Khanna S, Viji JC. Trop Gastroenterol 2003;24(1):25-6

Makharia GK, et al Trop Gastroenterol 2003;24(4):200-01Tyner R, Turett G. South Med J 2004;97(4):393-94

Shintaku M, et al. Arch Pathol Lab Med 2003;127:231-234

Other Causes of Acute Pancreatitis

Inflammatory bowel disease – Crohn’s (not 5 ASA) – 4-foldUlcerative colitis 1.5 fold

Ischemia – systemic lupus sickle cell crisis Preeclampsia-eclampsia

Toxins – carbofuran insecticides Organophosphates

Fan HC, et al. J Microbial Immunol Infect 2003;36(3):212-4Ahmed S,et al. Am J Hematol 2003 73(3):190-3

Parmar MS. JOP 2004;5(2):101-4Rizos E, et al. JOP 2004;5(1):44-7

Munk AM J Gastro 2004

Acute Pancreatitis

• Rare cause of acute pancreatitis

• Serum triglycerides usually >1000 mg/dL

• May cause chronic disease

• Can be drug-induced:

Alcohol, estrogens,isotretinoin, HIV-protease inhibitors

TG

TG lipase

Free fatty acids

Cell damage

Hypertriglyceridemia

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 2004;239(5):678-85

Adv Thr 2005;22:225

Mori A, 2003 DDS

Acute Biliary Pancreatitis

Goals are to identify:

1. patients whose stones have not passed

2. patients with complications of stones – cholangitis

ERCP is done only if there is biliary obstruction with cholangitis

Biliary Pancreatitis: What happens to CBD stones?

Stone or concretion is found in CBD

a) within 48 hours after admission in 62% – 75%

a) After 48 hours post admission CBD stones are found in 3% – 33%

The natural history of CBD stones is passage

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 2003;90:42-47

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


Acute Biliary Pancreatitis: First 24 to 48 hours

Jaundice with Bilirubin > 1.35 @ 24 hrs

ERCP MRCP

PosNeg

Stone removal

Elective surgical cholecystectomy

CBD stones

Neg Pos

Role of Surgery in Patients with Severe Acute Pancreatitis

Indication Timing

Biliary pancreatitis

Infected necrosis

Laparoscopic cholecystectomy during hospitalization or < 6 weeks after episodes

Later: > 10 days unless unstable with infected necrosis

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 1997;173:71-7

Buchler MW, et al Dig Dis 1992;10:354-62Mai G, et al Berlin, Blackwell Science 1999;475-85

ROLE OF PROPHYLACTIC ANTIBIOTICS IN PATIENTS WITH SEVERE ACUTE

PANCREATITIS

Adapted from H. Beger et al., Gastroenterology 1986; 91:433

Acute Pancreatitis

Timing of Pancreatic Infections

%Cases

0

20

40

60

80

100

< 7 days 7-14 days 14-21 days > 21 days

The incidence of pancreatic infections increases with time

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 1995;181:279-288

Rau B, et al. World j Surg 1997;21:155-161

Isenmann R, et al.Br J Surg 1999;86:1020-1024

Wilson PG, et al. J Antimicrob Chemother 1998;41(suppl A):51-63

Tenner S, et al. Gastroenterology 1997;113:899-903

Buchler MW, et al. Ann Surg 2000;232:619-626

Preoperative morbidity in patients with infected and sterile necrosis

Bacteriologically positive (45 pts)

n %

Bacteriologically negative (69 pts)

n %

P value

Cardiovascular complications (systemic Pa <80 mm Hg for > min 14 31.0 5 7.3 0.001*

Pulmonary insufficiency (Pa02<60mm Hg) 18 40.0 10 14.3 0.01

Renal insufficiency (creatinine >120 µM) 19 42.2 15 21.7 0.02Sepsis (rectal temperature >38.5°C; leukocytes <4,000 or >12,000/mm3; platelets <150,000/mm3: base excess >-4 16 35.6 6 8.7 0.001*Gastrointestinal bleeding 8 17.8 4 5.8 0.05

*P=0.05 by Holm’s rejective multiple test procedure

Ref: Beger, et al. Pancreatology 2005;5:10-19

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,

p=0.02) was demonstrated

Pancreatic sepsis showed an advantage for therapy (Odds ratio 0.51, p=0.04)

Extra-pancreatic infection could be evaluated in three studies, but showed no significant advantage for therapy (Odds ratio 0.47, p=0.05) Cochrane Database Syst Rev 2003;(4):CD002941

Antibiotic Therapy for Prophylaxis Against Infection of Pancreatic Necrosis in Acute Pancreatitis

(Cont) Surgery rates were not significantly reduced (Odds ratio

0.55, p=0.08)

Fungal infections showed no strongly increased preponderance with therapy (Odds ratio o.83, p=0.7)

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

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

Ciprofloxacin plus metronidazole vs. placebo in severe acute pancreatitis

Intention-to-treat analysis(114 patients)

Ciprofloxacin/ placeboMetronidazole (56 patients)(58 patients)

Necrotizing pancreatitis on contrast-enhanced CT scan(76 patients)

Ciprofloxacin/ placeboMetronidazole (35 patients)(41 patients)

MortalitySurgical treatmentInfected pancreatic necrosis

5% 7% 17% 11% 12% 9%

7% 11% 24% 19% 17% 14%

Isenmann R, et al. Gastroenterology 2004;126:997-1004

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 2004;1195-1198

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 2007;245;674-683

As Good As it Gets:The 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 2007;245 (5): 684-85

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


Severe Acute Pancreatitis – 2009

CT

No Necrosis Necrosis > 30%

No antibiotic

?AntibioticsMeropenem for 10-14 days

ESAP

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 2000;232(5):619-26Mier J, et al. Am J Surg 1997;173(2):71-5Rau B, et al. Br J Surg 1998;85(2):179-84

Infected NecrosisSuspicion

Tº > 100 F elevated WBC unresolved organ failure Recurrence of SIRS or persistence > 7 days

Diagnosis CT guided aspirate for gram stain and Culture and

sensitivity

Severe Acute Pancreatitis: Role of CT-guided Needle Aspiration

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 1981;26(7):585Freeny PC, et al AJR 1998;170:969-975

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 debridementPappas TN. Am J Gastroenterol 2005;100:2371-2374

Treatment Guideline V:Treatment of Infected Necrosis

CT-guided percutaneous aspiration with Gram’s stain and culture aspirate is recommended when infected necrosis is suspected

Treatment of choice in infected necrosis is surgical debridement

Level of Evidence III


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

Acute Pancreatitis: Nutrition

Route of Alimentation

Acute Pancreatitis

Negative effects of TPN Increased gut permeability Increased central catheter-related sepsis Immunosuppressive effects Increased incidence of septic complications Greatly increased costs

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 1974:67:975King BK, et al. Arch Surg

Kudsk KA, et al Ann Surg 1996:223:629Mochizuk H, et al Ann Surg 1984;200:297-310

Alverdy J, et al. Ann Surg 1985;202:681Schroeder D, et al JPEN 1991;15:376

Moore FA, et al. J Trauma 1989;29:916.

Safe and well-tolerated:Elemental diet causes less pancreas stimulation

Demonstrated Benefits:Reduced infectionsFewer metabolic complications

Shorter length of stay

Potential benefits: Improved intestinal permeability

Reduced systemic inflammatory response

Acute Pancreatitis: Nutrition

Enteral Feeding

Enteral Feeding

Marik PE BMJ 2004; doi:10.1136/bmj

Enteral vs Parenteral Nutrition Favors FavorsStudy enteral parenteral

Infection

0.1 1 10

Complications other than infection

Surgical interventions

Mortality

Acute Pancreatitis

Enteral vs Parenteral Nutrition

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, P=0.004), reduced surgical interventions to control pancreatitis (0.48, 0.22 to 1.0; P=0.05)

A reduced hospital stay (mean reduction 2.9 days, 1.6 days to 4.3 days, P<0.001)

There were no significant differences in mortality (relative risk ).66, 0.32 to 1.37, P=0.3) or non-infectious complications (0.61, 0.31 to 1.22, P=0.16) between the two groups Marik, PE, Zaloga GP. BMJ 2004;328:1407-09

Infections

Favors FavorsStudy enteral TPN

Abou-Assi

Gupta

Kalfarentzo

McClave

Olah

Windsor

0.01 0.1 1 10 100

Total (95% CI)

Marik PE, Zaloka GP. BMJ 2004; 328:1407

Nutritional Support and InfectionAcute Pancreatitis

Nutritional Support and Infection

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


Treatment Guideline I:Supportive 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


Positive

Suggestion of infection after day 5

Support and stabilize

Approach to Patients with Severe Acute Pancreatitis

.

Negative

Observe and re-aspirate

Organ system failure -Antibiotics ?

CT guided needle aspiration

Adjust Antibiotics

Stable

Follow

Unstable

Surgery

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Pancreatitis

Health & Medicine

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