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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Acute Liver Failure (ALF) is a devastating syndrome characterized by rapid deterioration of liver function in patients without pre-existing liver disease. It is defined by coagulopathy (INR ≥1.5) and hepatic encephalopathy occurring within 26 weeks. Its incidence is 1–6 cases per million per year, with a mortality rate of 40–80% without liver transplantation. We present the case of a 69-year-old female patient with stage 2A refractory Multiple Myeloma who developed ALF in the context of septic shock.
The patient presented to the emergency department with a 5 day history of cough, myalgia, asthenia, oliguria, diarrhea, general malaise, and abdominal pain. On admission, she had hypotension 70/40 mmHg, fever, tachycardia, somnolence, and jaundice. Evaluation revealed left lung consolidation and hepatic dysfunction (total bilirubin 14 mg/dL, AST 1250 U/L, ALT 980 U/L, INR 2.3), renal failure (creatinine 4.2 mg/dL), metabolic acidosis, and pancytopenia. She was admitted to the ICU with diagnoses of septic shock, ARDS, acute hepatic and renal injury (KDIGO stage 3), pancytopenia, and refractory myeloma. Subsequently, she developed acute cholecystitis requiring urgent cholecystectomy, complicated by severe coagulopathy and massive bleeding that necessitated surgical reintervention for hemostasis. Her clinical course worsened with increased hemodynamic instability, requiring high-dose vasopressors (norepinephrine 1 mcg/kg/min, epinephrine 0.5 mcg/kg/min), progressive liver and kidney failure (bilirubin 28.4 mg/dL, INR 3.4, creatinine 4.7 mg/dL) persistent pancytopenia, refractory metabolic acidosis, and capillary leak syndrome.
Extracorporeal support included Multiple-Pass Albumin Dialysis (MPAD) and Therapeutic Plasma Exchange (TPE). Three sessions led to marked biochemical improvement (creatinine 1.4 mg/dL, bilirubin 3.1 mg/dL), with continued decline Figure 1,2. Despite apparent hepatorenal recovery, on the 14th day she developed sudden malignant ventricular arrhythmia refractory to resuscitation, resulting in death.
The pathophysiology of ALF in sepsis involves hemodynamic disturbances with hepatic hypoperfusion, an exaggerated systemic inflammatory response, direct endotoxin toxicity, mitochondrial dysfunction, and intrahepatic cholestasis. Multiple myeloma acted as an aggravating factor due to immunosuppression, possible direct or indirect liver involvement, and subclinical hepatotoxicity from prior chemotherapy.
The therapeutic approach was based on three pillars: etiological treatment (infection source control and cholecystectomy), multi-organ support (hemodynamic, respiratory, metabolic, and hematologic), and extracorporeal therapies MPAD and TPE.
This case demonstrates the biochemical efficacy of combined extracorporeal therapy (MPAD + TPE) for hepatorenal support in a catastrophic ALF situation, achieving significant improvement that, however, was not enough to overcome a fatal cardiac complication. It highlights the potential of these techniques as a bridge to recovery or transplantation, but also underscores that in oncological patients with severe comorbidities, success depends on global stability and the control of all complications, not just hepatic ones. The death underscores the remaining challenges in managing this high-risk population.
