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Acute pancreatitis (AP) is an inflammatory disease of the pancreas that can lead to gland necrosis, and end‐organ failure in up to 20% of cases [1]. The disease is classified into three severity categories: mild, moderate, and severe pancreatitis [2]. Mild AP occurs when there is no organ failure or local complications such as fluid collection or necrotic collection. Moderately severe AP occurs in patients with transient organ failure (<48 hours duration) and/or acute fluid or necrotic collection and/or decompensation of a comorbid condition due to AP. Severe pancreatitis occurs when organ failure persists for more than 48 hours [2]. The mild category confers low morbidity and mortality, moderately severe implies high inpatient morbidity but low mortality, and severe portends high morbidity and mortality [2]. Given the prognostic implication of severity, early prediction of severe disease thus has been a subject of intense research [3,4].

Over the last several decades, over a dozen prediction tools have been developed using various clinical parameters including examination findings, radiological features, laboratory values, and host‐related characteristics [5–11]. Development of these tools paralleled advances in our understanding of some key pathophysiological markers and mediators of severe pancreatitis. For example, early intravascular volume deficit has long been shown to mediate progression of parenchymal injury to necrosis in animal models and humans [12,13]. This understanding informed exploration of surrogate markers of intravascular volume as predictors of severity, such as blood urea nitrogen and hemoconcentration [5,14]. It is well recognized that severity of host inflammatory response leads to end‐organ injury especially within the first two weeks of disease onset [1,15]. Therefore, investigators studied leukocytosis, elevated C‐reactive protein (CRP), and presence of systemic inflammatory response syndrome (SIRS) as predictors of severity [10,11]. Cytokines such as interleukin (IL)‐1β, IL‐6, IL‐8, and tumor necrosis factor (TNF)‐α have also been investigated as potential biomarkers of severity [16,17]. Prognostic significance of fat saponification and its binding to calcium led to calcium level being included in some of the scoring systems [18]. As with other illnesses, baseline reserve of vital organs has been shown to impact a patient’s probability of survival [19].

Existing prediction tools (Table 4.1) attempt to assess at least one or more of the following: (i) presence of volume deficit; (ii) severity of host inflammatory response; (iii) age and comorbidity burden; (iv) risk of fat saponification; and (v) early organ dysfunction. In this chapter, we discuss each of these pathophysiological mechanisms, and prediction tools that attempt to assess these early in the course of the disease. Advantages, disadvantages, and future direction are also discussed.