Acute pancreatitis: the substantial human and financial costs

Abstract

A greater understanding of the natural history of acute pancreatitis combined with greatly improved radiological imaging has led to improvement in the hospital mortality from acute pancreatitis, from around 25-30% to 6-10% in the past 30 years. Moreover, it is now recognised that the first phase of severe acute phase pancreatitis is a systemic inflammatory response syndrome (SIRS), during which multiple organ failure and death often supervene. Survival into the second phase may be accompanied by local complications, such as infected pancreatic necrosis, which may be prevented by prophylactic antibiotics and treated by judicious surgery. Intensive care unit costs can be substantial, but might be justified because of the excellent quality of life of survivors. Reduction in multiple organ failure by agents such as lexipafant, an antagonist of platelet activating factor (PAF) (which plays a critical role in generating the SIRS), may contribute to intensive care unit cost containment, as well as reducing the incidence of local complications and deaths from acute pancreatitis. A further improvement in the human and financial costs also requires the centralisation of the management of patients with severe acute pancreatitis, to single hospital units whose concentrated expertise equips them to intervene most effectively in what is still recognised as a highly complex disease.

Figure 1

Schematic representation of the important pathways in acute pancreatitis leading to systemic inflammatory response syndrome (SIRS) and multiple organ failure. PAF, platelet activating factor; IL, interleukin, TNF-α, tumour necrosis factor α; PGE₂, prostaglandin E₂; TXA₂, thromboxane A₂; LT₄, leukotriene series 4; IIs PLA₂, type II (non-pancreatic) secretory phospholipase A₂; NO, nitric oxide.

Figure 2

Rising mortality in acute pancreatitis with increasing number of organs affected (adapted from Heath et al²⁶).