European Gastroenterology & Hepatology Review, 2009;4(2):74-77
Acute pancreatitis (AP) is a localised inflammatory condition that may extend to peri-pancreatic tissue and other organs, inducing multiorgan dysfunction syndrome (MODS), with an increased mortality rate.1 The majority of patients present with mild disease; however, in approximately 20–25% of patients severe acute pancreatitis (SAP) develops. In 1925 Lord Moynihan described acute pancreatitis as "the most terrible of all the calamities that occur in connection with the abdominal viscera. The suddenness of its onset,the illimitable agony which accompanies it, and the mortality attendant upon it, all render it the most formidable of catastrophes."
Times have changed, but AP is still a common and potentially fatal disease with non-specific treatment and an unpredictable prognosis. Until now it has been a challenging disease to manage, with a significant burden of morbidity, a high mortality rate and a large financial cost. In spite of significant improvements in our understanding of the pathophysiology of the disease and advances in its diagnosis and management, the mortality rate has remained stable since the 1970s.2-4 While mild AP has a mortality rate below 1%, the rate may reach 10% in necrotising pancreatitis and up to 25% when pancreatic necrosis infection develops.5 In fulminant AP, a higher mortality rate ranging from 20 to 60% and even from 30 to 90% has been reported.6–8
Severity of Prognosis in Acute Pancreatitis
The management of AP differs according to the severity of the disease. Early, precise discrimination between patients likely or unlikely to have severe pancreatitis would be of great benefit in establishing proper therapy. Despite the importance of early prognosis, many patients initially identified as having mild disease progress to SAP over time.
Identification of severe cases during the first two to three days of symptoms, when MODS takes place, is difficult. The best predictors include clinical features, markers of pancreatic injury and markers of inflammatory response. In a meta-analysis of 399 patients presenting with AP, a serum haematocrit above 44%, body mass index (BMI) above 30kg/m2 and pleural effusion on chest X-ray were the most sensitive predictors of overall severity. The authors validated these criteria in a prospective cohort of 238 American patients. Known as the ‘panc 3 score’, it appears to be a new, simple stratification system.9
Single biochemical markers to predict severity are still found. Among them, interleukin (IL)-6 and procalcitonin (PCT) seem to be useful.10,11 A recent prospective, international, multicentre study revealed that monitoring of PCT allows for the early and reliable assessment of clinically relevant pancreatic infections and overall prognosis in AP. According to the authors, this single test parameter significantly contributes to an improved stratification of patients at risk of developing major complications.12
Disturbances of coagulation and fibrinolysis are known complications of AP.13,14 There are suggestions in the literature that some parameters of coagulation and fibrinolysis may correlate with the severity of disease. According to our data, D-dimer, protein S and protein C (PC) levels on the first and third day of AP are good prognostic factors. Specifically, D-dimer level increases early after onset of the disease seem to be a better prognostic factor than C-reactive protein (CRP).15,16 Others have found that PC deficiency and decreased activated PC (APC) generation in severe AP probably contribute to a compromised anticoagulant and anti-inflammatory defence.17 The PC pathway defects were associated with the development of multiorgan failure (MOF). These data support the usefulness of testing APC or PC and D-dimer levels to improve the clinical outcome in AP.17,18
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