Severe acute pancreatitis: Clinical course and management

Abstract

Severe acute pancreatitis (SAP) develops in about 25% of patients with acute pancreatitis (AP). Severity of AP is linked to the presence of systemic organ dysfunctions and/or necrotizing pancreatitis pathomorphologically. Risk factors determining independently the outcome of SAP are early multi-organ failure, infection of necrosis and extended necrosis (>50%). Up to one third of patients with necrotizing pancreatitis develop in the late course infection of necroses. Morbidity of SAP is biphasic, in the first week strongly related to early and persistence of organ or multi-organ dysfunction. Clinical sepsis caused by infected necrosis leading to multi-organ failure syndrome (MOFS) occurs in the later course after the first week. To predict sepsis, MOFS or deaths in the first 48-72 h, the highest predictive accuracy has been objectified for procalcitonin and IL-8; the Sepsis-Related Organ Failure Assessment (SOFA)-score predicts the outcome in the first 48 h, and provides a daily assessment of treatment response with a high positive predictive value. Contrast-enhanced CT provides the highest diagnostic accuracy for necrotizing pancreatitis when performed after the first week of disease. Patients who suffer early organ dysfunctions or at risk of developing a severe disease require early intensive care treatment. Early vigorous intravenous fluid replacement is of foremost importance. The goal is to decrease the hematocrit or restore normal cardiocirculatory functions. Antibiotic prophylaxis has not been shown as an effective preventive treatment. Early enteral feeding is based on a high level of evidence, resulting in a reduction of local and systemic infection. Patients suffering infected necrosis causing clinical sepsis, pancreatic abscess or surgical acute abdomen are candidates for early intervention. Hospital mortality of SAP after interventional or surgical debridement has decreased in high volume centers to below 20%.

Figures

Figure 1

Pattern of inflammation and systemic complications in acute pancreatitis.MAP: Mild acute pancreatitis; SAP: Severe acute pancreatitis; IAP: Intestinal oedematous pancreatitis; NP: Necrotizing pancreatitis; IN: Infected necrosis; SPN: sterile pancreatic necrosis; SIRS: severe inflammatory response syndrome; OF: Organ failure; MOD: Multiorgan failure; SEPSIS: Leukocytes > 10 000/mm3 + fever > 38.5 rectal/> 48 h + metabolic acidosis base excess > -4 mmol/L; MOFS: Multiorgan failure syndrome; ESAP: Early severe acute pancreatitis.

Figure 2

Relation between bacterial infection and extent of necrosis in 225 patients with severe acute pancreatitis. 1On the basis of contrast-enhanced CT. bP = 0.008 between the groups, Cochran-Armitage trend test.

Figure 3

Algorithm for clinical decision making in acute pancreatitis. AIP: Acute interstitial pancreatitis; NP: Necrotizing pancreatitis; CRP: C reactive protein; CECT: Contrast-enhanced computer tomography; LDH: Lactate dehydrogenase; ERC: Endoscopic retrograde cholangiography; ES: Endoscopic sphincterotomy; CE: Laparoscopic cholecystectomy; FNP: Fine needle procedure; MOF: Multiorgan failure syndrome.