Bacterial infection and extent of necrosis are determinants of organ failure in patients with acute necrotizing pancreatitis

Abstract

The incidence of organ failure is determined by both bacterial infection and extent of necrosis. The incidence of organ failure is determined by the extent of necrotic parenchyma in patients with sterile necrosis. Infected necrosis is associated with a high incidence of organ failure irrespective of the extent of necrosis.

Practice Guidelines in Acute Pancreatitis

“…Median prevalence of organ failure in necrotizing pancreatitis is 54% (range 29-78%) (31,50,54,82,83,120,147,148). Prevalence of organ failure is the same or somewhat higher in infected necrosis (34-89%) than in sterile necrosis (45-73%) (66,83,138,161).…”

“…For example, in one report, there was no sharp cutoff between interstitial and necrotizing pancreatitis (52). In three reports, APACHE-II scores were not statistically different among patients with sterile and infected necrosis (66,83,134). In one recent report, APACHE-II generated within the first 24 h had a positive predictive value of only 43% and negative predictive value of 86% for severe acute pancreatitis as compared to the 48-h Ranson score of 48% and 93%, respectively (53).…”

“…The mortality in the absence of organ failure is 0 (50,66,68,83), with single organ failure is 3% (range 0-8%) (66,83,163), with multisystem organ failure 47% (range 28-69%) (48,66,68,83,120,163,164).…”

“…In two studies, Table 6. APACHE II Score APACHE II score = (acute physiology score) + (age points) + (chronic health points) Acute Physiology Score the Ranson score was the same in sterile and infected necrosis (66,134).…”

Differential Effects of Caspase-1/Interleukin-1β–Converting Enzyme on Acinar Cell Necrosis and Apoptosis in Severe Acute Experimental Pancreatitis

“…Depending on the degree of intrapancreatic damage, remote organ failure, sepsis, and, finally, patient death are frequent complications observed in the course of this disease (Isenmann et al, 1999). Whereas the initiating events leading to the development of necrosis are still poorly understood, the subsequent infiltration of different leukocyte subsets into the damaged gland are claimed to be the major source for the release of various toxic mediators, such as proteolytic enzymes (Rinderknecht, 1994), oxygen free radicals (Poch et al, 1999;Rinderknecht, 1994), and cytokines (Fink and Norman, 1996).…”