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Dig Dis Sci DOI 10.1007/s10620-016-4248-5 EDITORIAL Prevention of the Paracentesis-Induced Circulatory Dysfunction (PICD) in Cirrhosis: Is the SPA Treatment Worthwhile? John Carl Hoefs 1 Received: 3 July 2016 / Accepted: 5 July 2016 O Springer Science+Business Media New York 2016 The older leading concept concerning ascites formation postulates an imbalance of oncotic and hydrostatic forces, with portal pressure pushing fluid into the peritoneal cavity opposed by the serum colloid osmotic pressure generated by albumin. When hydrostatic exceed oncotic forces, the abdominal cavity fills with fluid until a counterbalancing increase in abdominal pressure prevents further ascites formation. Furthermore, patients with ascites are almost perfectly separated from those without ascites on the basis of portal pressure (relative to the cardiac pressure) and serum albumin concentration [1] seeming to support this concept. According to this model, decreased intra-abdom- inal pressure due to fluid removal by paracentesis promotes fluid movement into the peritoneal cavity at the expense of the intravascular compartment, potentially resulting in catastrophic hypotension and renal failure. Since these events were thought to occur soon after paracentesis, the prevailing recommendation was for \2 L to be removed at any one time. Harmful effects from paracentesis were considered likely despite a large global clinical experience that had not identified a high incidence of hypotension or renal failure due to a common and routine clinical procedure. Two factors changed this view. The first was the description of oncotic-hydrostatic balance between serum and ascites [2–7] documenting an ‘‘abnormal balance’’ between colloid osmotic and hydrostatic pressure rather than an outright imbalance. In this model, the portal pres- sure gradient (portal pressure relative to intra-abdominal & John Carl Hoefs jchoefs@uci.edu Emeritus Professor, University of California, Irvine, Irvine, CA, USA pressure) was the major cause of ascites, as reflected in the serum to ascites albumin gradient (SAAG) both of which are unchanged after removing peritoneal fluid, during diuresis, or following albumin infusions [4, 5]. Thus, rapid formation of ascitic fluid was an unlikely consequence of paracentesis in this model although a fragile system sen- sitive to changes in intravascular volume might be pre- dicted. Furthermore, the model predicted the importance of the SAAG in the differential diagnosis of ascites, a widely accepted finding [4, 5] supporting the validity of this model. The second was data obtained from controlled trials that failed to document a major decrease in systemic blood pressure or an increased incidence of renal failure follow- ing paracentesis [7]. Indeed, control of ascites with para- centesis appeared safer than with diuretics [7]. Nevertheless, carefully controlled trials using sensitive hemodynamic measures did document statistically signifi- cant mild subclinical abnormalities such as alterations in plasma renin activity (PRA) and creatinine in some patients with tense ascites following complete fluid drainage or ‘‘total’’ paracentesis, usually days after the procedure and this is termed paracentesis-induced circulatory dysfunction (PICD) [8, 9]. Progressive renal failure or vascular collapse was not reported in these studies. Nonetheless, the concept of PICD became firmly established, with data supporting the concept that PICD could be prevented by salt-poor albumin (SPA) infusions [9]. The concern remained that some patients with PICD would deteriorate to the point that severe adverse clinical events occurred, justifying the expense of SPA infusions in all patients undergoing para- centesis. Furthermore, similar, but more pronounced alterations were present in the context of this fragile hemodynamic system such as spontaneous bacterial peri- tonitis, with hemodynamic improvement and increased survival attributed to concurrent SPA infusions [10]. Thus,