Necrotizing Pancreatitis - Dbaril 1g5wm

Necrotizing Pancreatitis Donald Baril Department of Surgery Grand Rounds Elmhurst Hospital Center February 25, 2004

Epidemiology  185,000 cases of acute pancreatitis/year in U.S.  Gallstone pancreatitis s 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 mortality rates 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 and pancreatic enzymes which leads to the exposure of pancreatic proenzymes to lysosomal enzymes leading to pancreatic autodigestion  Biliary pancreatitis  obstructing stone at ampulla allows bile to reflux into the pancreatic duct  obstructing stone at ampulla produces pancreatic duct hypertension

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  MR

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 to disruption of the normal pancreatic microcirulation  accuracy of > 90% when at least 30% glandular necrosis is present

Severity of pancreatitis based on CT findings

CT findings of necrotizing pancreatitis

CT findings of necrotizing pancreatitis

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 persistent biliary 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  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 develop local pancreatic infection  Mortality triples in the presence of infection from 10% to 30%

 Risk of infection increases with the amount of necrosis and the time 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-absorbable antibiotics  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 remains unproven but should be pursued in cases with MSOF unresponsive 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 and peripancreatic 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 the retroperitoneum  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