Abstract
Neutropenic patients with acute myeloid leukemia (AML) are at high risk for severe, multidrug-resistant infections. Sepsis due to carbapenem-resistant Pseudomonas aeruginosa (CRPA) in this population often leads to septic shock and acute respiratory distress syndrome (ARDS), with historically poor outcomes. CytoSorb™ hemoadsorption has been proposed as an adjunctive therapy for refractory septic shock, but evidence in hematologic malignancies remains limited. This report describes a 29-year-old male with newly diagnosed AML complicated by neutropenic fever, bacteremia due to CRPA, and subsequent hospital-acquired pneumonia progressing to ARDS. Despite multiple antibiotic regimens and aggressive intensive care management, including mechanical ventilation, prone positioning, and continuous renal replacement therapy (CRRT), the patient developed refractory septic shock with persistent lactic acidosis and elevated inflammatory markers. Early adjunctive CytoSorb hemoadsorption was initiated, guided by maximal CytoScore criteria, as part of a comprehensive supportive strategy. Following CytoSorb therapy, the patient demonstrated transient hemodynamic and biochemical improvement; however, profound neutropenia and multi-organ failure persisted. Microbiological clearance of CRPA was not achieved; given confirmed colistin susceptibility and unknown carbapenemase mechanism, a salvage combination of colistin plus ceftazidime-avibactam was employed. Transient hemodynamic improvement was observed after CytoSorb initiation; however, cytokine assays were not performed, and microbiological clearance was not achieved, precluding any mechanistic attribution to CytoSorb. This case highlights the complexity of managing CRPA sepsis and ARDS in neutropenic AML patients, and the challenges in attributing observed clinical improvement to CytoSorb therapy in the context of multiple simultaneous interventions. The absence of cytokine assays (e.g., IL-6, TNF-α) precludes any mechanistic attribution of observed changes to cytokine adsorption, and interpretation should remain descriptive rather than causal. Observed transient changes occurred amid simultaneous interventions (broad-spectrum antibiotics, CRRT, prone ventilation, corticosteroids, and filgrastim), precluding attribution to any single therapy, including CytoSorb. Given the fatal outcome and persistent CRPA positivity, the clinical impact of this observation is limited, and the generalizability of a single-case report is restricted. Cautious interpretation is warranted, and CytoSorb may be considered as part of a comprehensive care bundle rather than as a standalone solution. Alternative tetracycline-based combinations were reviewed but not adopted under our center's salvage protocol for this XDR presentation. Future studies are warranted to clarify its clinical benefit and optimal timing in this population.