B53-27 Posterior Reversible Encephalopathy Syndrome and Post-Lumbar Puncture Subarachnoid Hemorrhage in a Lung Transplant Recipient

Abstract Introduction Posterior reversible encephalopathy syndrome (PRES) is characterized by vasogenic edema predominantly involving the posterior circulation and is often associated with immunosuppressive therapy such as tacrolimus. Lung transplant recipients are at elevated risk due to hypertension, renal dysfunction, and high-dose immunosuppression. This case illustrates tacrolimus-induced PRES complicated by post-lumbar puncture subarachnoid hemorrhage (SAH), underscoring the need for vigilance in evaluating new neurologic symptoms in immunocompromised patients. Case Description A 61-year-old man with a history of bilateral lung transplantation presented with severe headache, nausea, vomiting, fever, confusion, and hypertensive emergency. Head CT and CT angiography were unremarkable. He was treated with nicardipine infusion, and tacrolimus was held due to suspected neurotoxicity. Lumbar puncture revealed xanthochromia, glucose 72 mg/dL, RBC 11,000/µL, and WBC 30 (76% neutrophils); cultures and HSV PCR were negative. Brain MRI showed T2 hyperintense signals in bilateral parietal and cerebellar hemispheres, consistent with PRES (Figure 1A). Tacrolimus was replaced with cyclosporine, and levetiracetam was initiated for seizure prophylaxis. Despite improvement in encephalopathy, the patient developed worsening back pain, tremors, and persistent headaches with gait instability. Repeat spine MRI revealed extensive subarachnoid hemorrhage extending from the lumbar region into the lower thoracic spine, confirmed on contrast imaging (Figure 1B). The findings were attributed to traumatic LP-related bleeding, likely exacerbated by concurrent aspirin use. Neurosurgery initiated dexamethasone, resulting in marked symptomatic improvement. Discussion This case highlights two distinct yet interrelated neurologic complications in a lung transplant recipient: tacrolimus-induced PRES and iatrogenic SAH. Tacrolimus neurotoxicity results from endothelial dysfunction and impaired cerebral autoregulation, often reversible with drug discontinuation and blood pressure control. However, subsequent lumbar puncture in anticoagulated or antiplatelet-treated patients can precipitate spinal SAH, producing prolonged or worsening headaches. Prompt imaging and recognition of red-flag symptoms after LP are essential to prevent permanent deficits. In transplant recipients, maintaining strict blood pressure control, monitoring neurotoxic drug levels, and balancing anticoagulation risk are critical to prevent dual neurologic insults. This case reinforces the need for multidisciplinary management and early neuroimaging in transplant patients with new neurologic symptoms. This abstract is funded by: None