[Septic pancreatic necrosis in intensive care]. / La necrosi pancreatica infetta in terapia intensiva.

BACKGROUND: Infected necrotizing pancreatitis is the most fulminant variety of this disease. The reported mortality is up to 50%. The haemodynamic features of cardiovascular instability has many similarities to sepsis syndrome, septic shock and multiple organ dysfunction syndrome (MODS). The purpose of this study is to review personal experience in the ICU (hospital of Varese) to determine etiology, treatment and complications. METHODS: Twenty patients treated since 1988 with infected necrotizing pancreatitis required surgical treatment and mechanical ventilation. RESULTS: The mortality rate was 60% and ICU-stay was 26.5 +/- 12.3 days, the median age was 54 +/- 13. Ranson's criteria at admission to the ICU was 6.6 +/- 1.2, Glasgow point was 4.6 +/- 1.2 (5.5 +/- 0.87 died, 3.2 +/- 0.8 survived p < 0.01), Baltazar score 6.2 +/- 2.1 (7.4 +/- 2.1 died, 5.5 +/- 0.9 survived p < 0.05) and SAPS II score 43.4 +/- 12.1 (50.1 +/- 7.8 died, 34 +/- 5.5 survived p < 0.01). The etiology was: gallstones (45%), alcoholism (15%), ERCP (15%) and idiopathic in 25%. Serum pancreatic amylase was 342 +/- 113.9 U/l (550 +/- 100 died, 155 +/- 60 survived p < 0.01), lipase was 334 +/- 176 U/l and transaminases GOT was 123 +/- 46 u/l (156 +/- 90 died, 29 +/- 7 survived p < 0.05). High initial amylase and GOT levels were frequently found in non survived patients. MODS occurred in 17 cases (85%), ARDS in 2 patients (10%), abdominal bleeding in 6 (30%) and septic syndrome in 8 (40%). CONCLUSIONS: It is thus possible that a target-oriented approach including fluid replacement, rapid correction of intestinal underperfusion, inotropic and antibiotic therapy, supply of specific nutrients and other therapeutic strategies as open laparostomy must be employed to prevent MODS or septic syndrome in pancreatic infection after acute necrotizing pancreatitis.

Effect of recombinant IL-1 beta and recombinant gamma interferon on septic acute lung injury in mice.

The effect of recombinant human interleukin 1B (IL-1B) and recombinant human gamma interferon (IFN-g), when given prophylactically, in a mouse model of septic acute lung injury was studied. Mice were treated with various doses of IL-1B and IFN-g for 3 consecutive days prior to administration of lipopolysaccharide of Escherichia coli (1 mg/kg given intraperitoneally). To determine the histologic changes occurring after prophylactic administration of such cytokines, a scoring system was assessed. A significant reduction of edema and neutrophil accumulation into the lungs of mice was observed, especially at doses of 100 U per mouse and 10,000 U per mouse of IL-1B and IFN-g, respectively. Prophylactic administration of IL-1B or IFN-g caused histologic changes, including marked reduction of edema and neutrophil accumulation in the interstitial and alveolar spaces. Combined prophylactic administration of IL-1B and IFN-g provoked a marked decrease of neutrophil accumulation into the lungs, but was not accompanied by significant reduction of edema or hemorrhage. These results provide evidence for the beneficial role of IL-1B and IFN-g in the abnormality of septic acute lung injury by reducing inflammatory lesions.