PART III CHAPTER 12
Several prognostic scoring systems are used to predict the severity of acute pancreatitis in the first days of admission: among them are APACHE-ll, (Modified) Glasgow (Imrie) score, Ranson score, procalcitonin, C-reactive protein and blood urea nitrogen (BUN).15 These prognostic scoring systems are mainly used for severity stratification in clinical studies, and one can argue about their importance in daily clinical practice. Theoretically, severe acute pancreatitis is divided in a biphasic clinical course. The first phase (i.e., up to 1 to 2 weeks after onset of symptoms) is characterized by a proinflammatory immune response. A systemic inflammatory response syndrome (SIRS) often occurs, which is frequently accompanied by failure of one or more organ systems.16-18 Organ failure develops in around 40% of patients with severe acute pancreatitis and is associated with a mortality rate of approximately 30%.14,19 More than half of the cases of organ failure occur in the first week of admission.14 Patients with persistent organ failure or multi-organ failure have a worse prognosis than patients with transient organ failure or single organ failure.3,16,20 It has been suggested that approximately half of the deaths from necrotizing pancreatitis are caused by multi-organ failure in the early phase.14,20,21 In the second phase of the disease (i.e., after 1 to 2 weeks from onset of symptoms) the pro-inflammatory immune response usually subsides. In this phase, the patient’s immune system is probably suppressed which renders patients more susceptible to infectious complications caused by bacterial translocation.22-24 The most severe infectious complication in necrotizing pancreatitis is infection of pancreatic or peripancreatic necrosis. The incidence of infected necrosis in patients with necrotizing pancreatitis has remained stable over the last decades (around 30%).14,25 The peak incidence of infected necrosis is between 2 and 4 weeks after onset of disease.26 Infected necrosis is typically suspected when there is persistent sepsis, new onset sepsis or progressive clinical deterioration (i.e., signs of sepsis) despite maximal support in the second phase of the disease, without another source of infection. A pathognomonic sign of infected necrosis are impacted peripancreatic or intrapancreatic gas bubbles in a collection on CECT (Figure 2), although this is present in only a minority of patients. In some patients, gas bubbles can also be explained by a fistulous communication between the collection and bowel. Which however, also means the collection is contaminated. A fine needle aspiration (FNA) for microbiological culture can be performed to diagnose infected necrosis. However, FNA might not always be necessary in patients with necrotizing pancreatitis and suspected infected necrosis. In addition, FNA is associated with a risk of false-negative results.27 Because “suspected infected necrosis” no longer represents an immediate indication for invasive treatment, a FNA culture result will not per se guide clinical decision making. Intervention is generally postponed to 3 to 4 weeks after onset of disease, and the need for intervention is primarily dictated by clinical deterioration and encapsulation of the infected collection rather than a positive microbiological culture obtained by FNA. A recent Dutch multicenter randomized 230