The Rationale for Hemoadsorption in the Critically Ill: Sepsis and Beyond

Abstract List

19 Sep 2026 12:45 13:30
Zsolt MolnárHungary Speaker Managing Patients with Sepsis: modifying the course with ECOSA dysregulated host response to infection is central to the pathophysiology of sepsis and may culminate in life-threatening organ dysfunction. Given that this process is largely characterized by concurrent pro- and anti-inflammatory activation, immunomodulatory strategies have long been explored in sepsis research. Among these, extracorporeal removal of circulating cytokines, inflammatory mediators and other soluble factors through non-specific hemoadsorption with macroporous styrene-divinylbenzene sorbents has been proposed as a potential therapeutic approach. Its adoption into clinical practice has largely been based on pathophysiological considerations rather than on evidence from large, well-designed randomized clinical trials. Over the past 15 years, most of the available evidence has been predominantly derived from small, single-center cohorts, reports from registries and heterogeneous prospective studies with substantial variability in patients’ selection, timing, and treatment intensity. In addition, the precise mechanisms of action of hemoadsorption remain incompletely understood. Although several meta-analyses have attempted to synthesize the existing data, the overall quality and heterogeneity of the included studies limit the strength and reliability of their conclusions. As a result, current guideline recommendations are largely based on expert opinions rather than high-certainty evidence. This presentation aims to provide a concise overview of the biological rationale, current evidence, and contemporary clinical practice related to hemoadsorption in sepsis.Multimodal individualized hemodynamic managementAchieving hemodynamic stability in the critically ill patents has a pivotal role in ensuring positive outcomes. The pathomechanism is complex and include impaired myocardial contractility, relative or absolute intravascular hypovolaemia, bradycardia, and thus eventually impaired blood flow. Arterial pressure can be monitored continuously, which makes it the most important and feasible tool to assess circulation in real time. A given level of the mean arterial pressure (MAP) is often regarded as the main target to be normalized in several guidelines. However, it is not the sole determinant of organ perfusion pressure and, although coupled to blood flow, is not a surrogate of blood flow or tissue perfusion. Conversely, normotension does not guarantee adequate organ blood flow and may just mimic ‘occult hypoperfusion’. Therefore, achieving hemodynamic coherence between macro- and microcirculation should be our pivotal aim during resuscitation and hemodynamic management. This requires a complex approach that is called multimodal, individualised, contextualised management that takes into account all measurable components of oxygen delivery and consumption, organ perfusion and cardiac output. How to do it at the bedside, will be presented on this lecture.