Abstract: TH-PO0777
Role of Early vs. Delayed Polymyxin B Hemoperfusion (PMX-HP) Treatment in Viral Septic Shock
Session Information
- AKI: Critical Care, CKRT, Cardiorenal Syndromes, and Clinical Outcomes
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Khan, Sobia, Stony Brook University, Stony Brook, New York, United States
- Kim, Chang Kyung, UPMC, Pittsburgh, Pennsylvania, United States
- Mallipattu, Sandeep K., Stony Brook University, Stony Brook, New York, United States
Introduction
Endotoxin (Lipopolysaccharide) is a component of gram-negative bacterial outer wall, which has been investigated and acknowledged as one of the triggers of lethal shock during sepsis and drivers of cytokine storm. PMX-HP is an extracorporeal therapy which removes circulating cytokines and endotoxins (EA). While elevation in EA occurs because of gram-negative bacteremia, high levels have been reported to occur independent of gram-negative bacteremia, suggesting potential for endotoxin translocation across a dysfunctional gastrointestinal barrier.
Case Description
We describe two critically ill patients with severe SARS-CoV-2 infection with septic shock, Multiple Organ Dysfunction Score (MODS) ≥9 and elevated endotoxin activity (EAA 0.6–0.9). Neither patient had evidence of gram-negative bacteremia but had high endotoxin levels. Both received two 2-hour PMX-HP sessions, 24 hours apart.
Patient 1 received PMX-HP early during ICU admission, which resulted in reduced vasopressor requirement, improved oxygenation, lower MODS score, successful extubation, and eventual discharge from Intensive care unit.
While Patient 2 received PMX-HP later, after progression to advanced multiorgan failure. Although endotoxin levels decreased, the patient continued to deteriorate with refractory shock, worsening respiratory failure and ultimately death.
Both patients showed substantial reductions in endotoxin activity following PMX-HP (Patient 1: EA 0.72→0.45; Patient 2: EA 0.85→0.33). However, clinical outcomes differed significantly based on timing of therapy.
Discussion
These cases suggest that endotoxin activity contributed to organ dysfunction. Though PMX-HP consistently reduced endotoxin burden in both patients, meaningful clinical improvement was noted with earlier intervention before advanced multiorgan failure. Patients with high EA levels should be considered prior to developing severe symptoms as these populations may be more likely to reverse endotoxin-mediated damages.
Fold changes in inflammatory markers of patient 1 & 2 pre- and post-PMX-HP.