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8/2/2019 Necrotizing Pancreatitis - DBaril
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Necrotizing Pancreatitis
Donald Baril
Department of Surgery Grand Rounds
Elmhurst Hospital CenterFebruary 25, 2004
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Epidemiology
185,000 cases of acute pancreatitis/year in U.S.
Gallstone pancreatitis accounts for 40-80% of cases
Necrosis present in 20-30% of all cases
Most common between the ages of 50 and 70
Presence of necrosis increases morbidity and mortalityrates from 23% to 82% and <1% to 10% respectively
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Etiology
Gallstones
Alcohol abuse
Endoscopic retrograde cholangiopancreatography
Hyperlipidemia
Drugs
Pancreas divisum
Abdominal trauma
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Pathophysiology
Disruption in the normal separation of lysosomal andpancreatic enzymes which leads to the exposure of pancreatic proenzymes to lysosomal enzymes leading topancreatic autodigestion
Biliary pancreatitis
obstructing stone at ampulla allows bile to reflux intothe pancreatic duct
obstructing stone at ampulla produces pancreatic ducthypertension
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Presentation and Diagnosis
History: Epigastric pain, nausea/vomiting, fever
Physical exam: fever, tachycardia, epigastric tenderness,
Grey-Turner’s sign, Cullen’s sign
Laboratory values: elevated amylase and lipase, leukocytosis,
elevated liver function tests
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Radiographic studies
Abdominal x-ray
typically nonspecific
may exclude other causes of abdominal pain
may show a sentinel loop or a “colon cutoff sign”
Ultrasound
typically shows a diffusely enlarged,hypoechoic pancreas
sensitivity of 67% and near 99% specificity in
the diagnosis of acute pancreatitis
MRCP
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Colon cutoff sign
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Radiographic studies – CT scan
CT (contrast-enhanced) gold standard for the noninvasive diagnosis of
necrotizing pancreatitis
affected portions fail to enhance secondary todisruption of the normal pancreatic microcirulation
accuracy of > 90% when at least 30% glandularnecrosis is present
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Severity of pancreatitis based on CT findings
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CT findings of necrotizing pancreatitis
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CT findings of necrotizing pancreatitis
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CT findings of necrotizing pancreatitis
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Endoscopic retrograde cholangiopancreatography
Gold standard to diagnose choledocholithiasis
Should be used in combination with sphincterotomy for patients
with severe gallstone pancreatitis and suspected persistentbiliary obstruction
Carries inherent risks of exacerbating the ongoing pancreatitis
and introducing infection into sterile necrosis
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Management aims
Two phases of acute pancreatitis
Initial 14 days characterized by the systemic inflammatory
response syndrome (SIRS)
intensive medical support
prevention of infection
Infection of pancreatic necrosis which occurs in the second
and third week following the onset of symptoms
treatment of local infectious complications
and debridement
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Infected necrosis
30-70% of patients with acute necrotizing pancreatitis developlocal pancreatic infection
Mortality triples in the presence of infection from 10% to 30%
Risk of infection increases with the amount of necrosis and thetime from onset of pancreatitis
24% of pts have bacterial contamination at 1week
71% of pts have bacterial contamination at 3weeks greatest risk in pts with >50% necrosis
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Infected necrosis
Sources of infection include bacterial translocation from the
colon, hematogenous spread, descending infection via the
biliary duct system, or ascending via the duodenum
Organisms
Escherichia coli, Pseudomonas, Klebsiella,
Enterococcus, Proteus, Bacteroides
Streptococcus faecalis, Staphylococcus aureus Candida species
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Prevention of bacterial infection
Enteral feeding
avoids central line-related infections
maintains gut barrier integrity
decreases bacterial translocations
Selective decontamination of the gut with non-absorbableantibiotics
Prophylactic systemic antibiotics
Imipenem remains the antibiotic of choice
Quinolones in combination with Metronidazole are the
second-line agents
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Determination of infected necrosis
CT or ultrasound guided fine-needle aspiration of pancreatic
necrosis is performed in patients with known necrosis who
develop clinical signs of sepsis
sensitivity of 96% and specificity of 99%
complications include risk of secondary infection,
bleeding, and aggravation of acute pancreatitis
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Indications and timing of surgery
Benefit of surgery in patients with sterile necrosis remainsunproven but should be pursued in cases with MSOFunresponsive to medical treatment
Infected necrosis is a clear indication for surgery
Surgical intervention should be postponed as long as possible
demarcation between viable and necrotic tissue is
more clearly defined decreases the bleeding risk
minimizes surgery-related loss of vital tissue
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Goals of Surgical Interventions
1) Removal of pancreatogenic exudate from the peritoneal
cavity and lesser sac
2) Removal of infected, necrotic pancreatic andperipancreatic tissue
3) Preservation of viable pancreatic tissue
4) Postoperative evacuation of remaining debris and exudate
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Surgical Interventions
1) Necrosectomy with open packing
mortality of 15-17%
pancreatic fistula rate of 26-46%
2) Necrosectomy with closed packing
mortality of 6.2%
pancreatic fistula rate of 9%
3) Necrosectomy with closed continuous lavage of theretroperitoneum
mortality of 21%
pancreatic fistula rate of 19%
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Percutaneous drainage
Generally fails to be curative but may be beneficial in
stabilizing septic patients
Single study utilizing large bore drainage catheters (28 French)
avoided surgery in 47% of pts (16/34) with infected pancreatic
necrosis
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Complications of necrotizing pancreatitis
Persistent or recurrent infection
Postoperative hemorrhage
Pancreaticocutaneous fistula
Enterocutaneous fistula Duodenal obstruction
Pancreatic insufficiency
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Conclusions
Necrotizing pancreatitis continues to have significant morbidity
and mortality despite advances in medical therapy
Patients with necrotizing pancreatitis should all receive
antibiotic prophylaxis
Surgery should be delayed as long as possible and has no
proven role in sterile necrosis
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