Necrotizing Pancreatitis - DBaril

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Necrotizing Pancreatitis

Donald Baril

Department of Surgery Grand Rounds

Elmhurst Hospital CenterFebruary 25, 2004



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



Etiology

Gallstones

Alcohol abuse

Endoscopic retrograde cholangiopancreatography

Hyperlipidemia

Drugs

Pancreas divisum

Abdominal trauma



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



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



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



Colon cutoff sign



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



Severity of pancreatitis based on CT findings



CT findings of necrotizing pancreatitis



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



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



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



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



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



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



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



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



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%



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



Complications of necrotizing pancreatitis

Persistent or recurrent infection

Postoperative hemorrhage

Pancreaticocutaneous fistula

Enterocutaneous fistula Duodenal obstruction

Pancreatic insufficiency



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

Necrotizing Pancreatitis - DBaril

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