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Hemodynamic failure in AP has been defined as systolic blood pressure of less than 90 mmHg despite adequate volume administration [4]. In clinical practice, shock in a patient with AP is usually a consequence of two different situations that may coexist: a hypovolemic state (hypovolemic shock), and systemic arteriolar vasodilation (distributive shock). Cardiac damage and dysfunction have been described in patients with the most severe forms of AP [20,21] but are less frequent; it should be considered if an important hemodynamic impairment is present.

1 Hypovolemic shock. A hypovolemic state is frequent in patients with AP, especially in patients with moderate‐to‐severe disease [22]. There are several factors determining this hypovolemia: reduction in oral intake, fluid sequestration due to the development of an important third space (interstitial edema, retroperitoneal collections, pleural effusion, paralytic ileus), and increased losses (vomiting, diaphoresis, tachypnea) [22]. Vascular leak syndrome, an increase in vascular permeability due to mediators like angiopoietin‐2, may be important in this regard [23]. Much less frequently, patients with local complications may have retroperitoneal or gastrointestinal bleeding, which can be life‐threatening.

2 Distributive shock. Arteriolar tone may decrease due to uncontrolled secretion of proinflammatory mediators. As stated, it can result from the initial aseptic inflammation of the pancreas, or be due to infections.

It has been hypothesized that early and accurate volume replacement could stabilize the permeability of the capillary membrane and support the macro‐ and micro‐circulation, prevent the cascade of events leading to pancreatic necrosis, maintain the function of the intestinal barrier, and modulate the inflammatory response [24], but evidence about the optimal volume and rate of fluid resuscitation from randomized controlled trials is lacking [25]. Studies addressing fluid resuscitation in severe AP are scarce, and most of them are retrospective with small sample sizes. Two randomized controlled studies from the same group investigated the effect of a more aggressive versus a moderate fluid resuscitation rate, and both showed decreased survival in patients receiving the aggressive strategy [26,27]. For this reason, aggressive fluid resuscitation in patients with established severe AP should be avoided, unless strictly needed. According to two randomized controlled trials, lactated Ringer’s solution has an anti‐inflammatory effect [28,29], but these studies were underpowered to detect improved survival or decreased incidence of organ failure.

Bearing in mind the limited evidence from the literature, we recommend lactated Ringer’s solution‐based fluid resuscitation, with an initial bolus of 10–20 ml/kg and a subsequent infusion of 1.5 to 3 ml/kg per hour, monitored with hematocrit (maintained between 35 and 44%), blood urea nitrogen plasma levels (an increase in serial blood tests may indicate the need for a more aggressive strategy), and urine output (>1 ml/kg per hour) [26,27,30]. These parameters should be monitored every 8–12 hours. Although the study of Wu et al. [28] did not demonstrate significant differences between standard and goal‐directed fluid resuscitation, the study was underpowered. In the case of organ failure, the patient should be monitored in an ICU setting. In the article of Sun et al. [31], patients monitored with pulse indicator continuous cardiac output (PiCCO) received more volume infusion, with lower need for renal replacement therapy and shorter ICU length of stay, but without differences in mortality. In the absence of higher‐quality studies, it seems logical to recommend strict hemodynamic monitoring in patients with shock or renal failure, using thermodilution and/or ultrasound techniques [32].

Once adequate volume replacement is completed, if hemodynamic impairment persists, norepinephrine infusion should be started in order to normalize peripheral vascular resistances. Once again, strict hemodynamic monitoring is recommended in the management of these cases. The use of corticosteroid therapy has been tested in several randomized trials involving small sample sizes. According to a meta‐analysis, corticosteroid therapy for AP with shock and high norepinephrine requirements may be associated with reductions in length of hospital stay, need for surgical intervention, and mortality rate [33], but further research is needed before recommending this treatment.