New tools for optimizing fluid resuscitation in acute pancreatitis

Abstract

Acute pancreatitis (AP) is a frequent disease with degrees of increasing severity responsible for high morbidity. Despite continuous improvement in care, mortality remains significant. Because hypovolemia, together with microcirculatory dysfunction lead to poor outcome, fluid therapy remains a cornerstone of the supportive treatment. However, poor clinical evidence actually support the aggressive fluid therapy recommended in recent guidelines since available data are controversial. Fluid management remains unclear and leads to current heterogeneous practice. Different strategies may help to improve fluid resuscitation in AP. On one hand, integration of fluid therapy in a global hemodynamic resuscitation has been demonstrated to improve outcome in surgical or septic patients. Tailored fluid administration after early identification of patients with high-risk of poor outcome presenting inadequate tissue oxygenation is a major part of this strategy. On the other hand, new decision parameters have been developed recently to improve safety and efficiency of fluid therapy in critically ill patients. In this review, we propose a personalized strategy integrating these new concepts in the early fluid management of AP. This new approach paves the way to a wide range of clinical studies in the field of AP.

Keywords: Central venous pressure; Fluid; Pancreatitis; Passive leg raising; Preload.

Figure 1

Suggested algorithm for fluid management in acute pancreatitis. AP: Acute pancreatitis; MAP: Mean arterial pressure; HR: Heart rate; ScvO₂: Central venous oxygen saturation; UO: Urinary output; SV: Stroke volume; PP: Arterial pulse pressure; PLR: Passive leg raising; CVP: Central venous pressure; FC: Fluid challenge.

Figure 2

Schematic representation of central venous pressure/stroke volume of normal (solid line) and failing heart (dotted line). When the heart is fluid responsive, a fluid challenge induces a large increase in stroke volume (SV) and a small increase in central venous pressure (CVP). When the heart is fluid unresponsive, a fluid challenge induces a small increase in SV and a large increase in CVP. In contrast, there is no reliable threshold of CVP that can be used in current practice to predict a positive or negative response to fluid loading. This threshold depends mostly on the cardiac function at the time of fluid infusion.