C48-04 Fatal Autonomic Failure in Guillain-Barré Syndrome Following IVIG-Associated TRALI

Guillain-Barré Syndrome (GBS) is an acute immune-mediated polyneuropathy that can rapidly progress to respiratory failure and autonomic instability. While intravenous immunoglobulin (IVIG) is a cornerstone of treatment, it carries rare risks, including transfusion-related acute lung injury (TRALI). We report a fatal case of GBS in a 48-year-old male complicated by IVIG-associated TRALI, persistent encephalopathy, and severe autonomic failure. The patient presented with progressive bilateral lower extremity weakness following recent gastrointestinal and respiratory symptoms. Neurologic evaluation suggested acute inflammatory demyelinating polyneuropathy (AIDP). Within 24 hours, weakness progressed to involve the upper extremities and respiratory muscles, prompting intubation. IVIG was initiated after lumbar puncture. Following the second IVIG dose, the patient developed acute respiratory decompensation with hypoxemia, fever, and bilateral wheezing. Imaging and cardiac assessment ruled out fluid overload or cardiac dysfunction. These findings met the clinical criteria for TRALI. IVIG was discontinued, and plasmapheresis initiated, resulting in transient respiratory improvement. Despite stabilized oxygenation, the patient remained unresponsive. Over subsequent days, he developed profound autonomic dysregulation—marked by fluctuating blood pressure, heart rate variability, and central hyperthermia peaking at 41.2 °C—unresponsive to antipyretics and external cooling. These findings indicated severe central autonomic failure. Despite optimal supportive measures, including sedation management, targeted temperature control, and continued ventilatory support, the patient’s condition deteriorated. He ultimately succumbed to complications from fulminant GBS with irreversible autonomic failure. This case highlights two critical and potentially fatal complications in GBS. First, TRALI is a rare but serious adverse reaction to IVIG, typically occurring within six hours of infusion. It presents with hypoxemia, fever, and non-cardiogenic pulmonary edema. Prompt recognition and discontinuation of the offending agent are essential. In this patient, clinical suspicion led to early cessation of IVIG and transition to plasmapheresis, likely preventing further pulmonary compromise. Second, autonomic instability—including labile vitals and refractory central fever—is a known but often underrecognized complication of severe GBS. In this case, it proved catastrophic and unresponsive to intensive supportive therapy. Clinicians should remain vigilant for both disease- and treatment-related complications in GBS. Early recognition of TRALI and severe autonomic dysfunction may guide timely interventions. Plasmapheresis may be a safer alternative for patients at risk of IVIG-associated complications. Central fever and autonomic collapse should be viewed as markers of poor prognosis in fulminant GBS. Despite appropriate interventions, this case tragically illustrates the potentially fatal trajectory of severe GBS. This abstract is funded by: none