Patients presenting with acute pancreatitis are often hypovolemic as a result of vomiting, reduced oral intake, third spacing of fluids, and diaphoresis. In fact, one expert has written that the minimal intravenous fluid requirements of a 70kg person during the first 48 hours after admission is 6 Litres without considering intravascular fluid sequestration loss. In addition, it is believed that the release of cytokines, chemokines, neutrophils, and macrophages leads to a pro-inflammatory state causing local...
Patients presenting with acute pancreatitis are often hypovolemic as a result of vomiting, reduced oral intake, third spacing of fluids, and diaphoresis. In fact, one expert has written that the minimal intravenous fluid requirements of a 70kg person during the first 48 hours after admission is 6 Litres without considering intravascular fluid sequestration loss. In addition, it is believed that the release of cytokines, chemokines, neutrophils, and macrophages leads to a pro-inflammatory state causing local and systemic inflammation. Such inflammation increases vascular permeability, which can lead to hypoperfusion and third spacing of fluids. Patients with acute pancreatitis are usually severely fluid depleted secondary to third spacing, also known as a capillary leak, and vomiting. The hypovolemia and circulatory shock cause preferential diversion of blood from the splanchnic circulation to increase cardiac output and ensure adequate perfusion of vital organs. Despite the ability of the intestine to increase oxygen extraction from the blood, prolonged hypoperfusion causes intestinal ischemia. This, in turn, leads to increased gut permeability and translocation of gut flora into the circulation perpetuating the already existing SIRS and predisposing to infection. Srinivasan also states that following fluid resuscitation, adequacy of splanchnic perfusion is the last to be restored, and hence intestinal ischemia may well persist despite the patient appearing well hydrated.
